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 The Cambridge Handbook of
Anxiety and Related Disorders

Edited by
Bunmi O. Olatunji
Vanderbilt University

Published online by Cambridge University Press

 The Cambridge Handbook of Anxiety and Related Disorders

This handbook surveys existing descriptive and experimental approaches to

the study of anxiety and related disorders, emphasizing the provision of
empirically guided suggestions for treatment. Based upon the findings from
the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), the
chapters collected here highlight contemporary approaches to the classifica-
tion, presentation, etiology, assessment, and treatment of anxiety and related
disorders. The collection also considers a biologically informed framework
for the understanding mental disorders proposed by the National Institute of
Mental Health’s Research Domain Criteria (RDoC). The RDoC has begun
to create a new kind of taxonomy for mental disorders by bringing the
power of modern research approaches in genetics, neuroscience, and
behavioral science to the problem of mental illness. The framework is a
key focus for this book as an authoritative reference for researchers and
clinicians.

bunmi o. olatunji, ph.d., is a professor in the Department of

Psychology and Psychiatry at Vanderbilt University, USA, where he also
serves as the Director of Clinical Training. He is Associate Editor of the
Journal of Consulting and Clinical Psychology.

Published online by Cambridge University Press

Published online by Cambridge University Press
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Information on this title: [Link]/9781107193062
DOI: 10.1017/9781108140416
© Cambridge University Press 2019
This publication is in copyright. Subject to statutory exception
and to the provisions of relevant collective licensing agreements,
no reproduction of any part may take place without the written
permission of Cambridge University Press.
First published 2019
Printed in the United Kingdom by TJ International Ltd. Padstow Cornwall
A catalogue record for this publication is available from the British Library.
Library of Congress Cataloging-in-Publication Data
Names: Olatunji, Bunmi O., editor.
Title: The Cambridge handbook of anxiety and related disorders / edited by Bunmi
Olatunji, Vanderbilt University, Tennessee.
Description: Cambridge, United Kingdom ; New York, NY, USA : University Printing
House, 2019. | Includes bibliographical references.
Identifiers: LCCN 2018024059 | ISBN 9781107193062
Subjects: LCSH: Anxiety – Handbooks, manuals, etc. | Anxiety disorders – Handbooks,
manuals, etc.
Classification: LCC RC531 .C355 2019 | DDC 616.85/22–dc23
LC record available at [Link]
ISBN 978-1-107-19306-2 Hardback
Cambridge University Press has no responsibility for the persistence or accuracy of
URLs for external or third-party internet websites referred to in this publication
and does not guarantee that any content on such websites is, or will remain,
accurate or appropriate.

Published online by Cambridge University Press

 To Eun Ha, Aiden, and Mitchell for all the inspiration that I will ever need

Published online by Cambridge University Press

Published online by Cambridge University Press
 Contents

List of Contributors page x

Anxiety and Related Disorders: An Introduction

rebecca c. cox and bunmi o. olatunji 1

Section 1 Basic Mechanisms in Fear and Anxiety 11

1 Learning Mechanisms in Fear and Anxiety: It Is Still Not What You
Thought It Was
sara scheveneels, yannick boddez, and dirk hermans 13
2 Attentional Bias and the Anxiety Disorders
ernst h. w. koster and anouk vanden bogaerde 41
3 Perceptual Mechanisms of Anxiety and Its Disorders
wen li 59

Section 2 Transdiagnostic Processes 89

4 Neuroticism/Negative Affectivity
david watson 91
5 Anxiety Sensitivity
norman b. schmidt, nicole short, ian stanley, nicholas
allan, and brian albanese 121
6 Disgust Proneness
kelly a. knowles and bunmi o. olatunji 163
7 Intolerance of Uncertainty
peter m. mcevoy, r. nicholas carleton, kelly correa,
stewart a. shankman, and sarah shihata 196
8 Distress Tolerance
lance m. rappaport, erin c. berenz, carl lejuez,
and roxann roberson-nay 227

vii

Published online by Cambridge University Press

 viii Contents

9 Experiential Avoidance
fallon r. goodman, maria a. larrazabal, john t. west,
and todd b. kashdan 255
10 Emotion Regulation
katya c. fernandez, amanda s. morrison,
and james j. gross 282

Section 3 Assessment, Diagnosis, and Cultural

Manifestations of Anxiety and Related Disorders 307
11 Anxiety Disorders
anthony j. rosellini, esther s. tung, and
timothy a. brown 309
12 Obsessive-Compulsive and Related Disorders
andrew m. kiselica and eric a. storch 349
13 Trauma- and Stressor-Related Disorders
daniel j. lee, sarah e. kleiman, and
frank w. weathers 371
14 Cultural Considerations in Anxiety and Related Disorders
devon hinton and eric bui 394

Section 4 Etiology and Phenomenology of Specific

Anxiety Disorders 419
15 Specific Phobia
peter j. castagna, marie nebel-schwalm, thompson
e. davis iii, and peter muris 421
16 Panic Disorder and Agoraphobia
bethany a. teachman, miranda l. beltzer,
and alexandra j. werntz 451
17 Social Anxiety Disorder
arielle horenstein, rachel m. butler, and richard
g. heimberg 480
18 Generalized Anxiety Disorder
ki eun shin, lucas s. lafreniere, and michelle g. newman 517
19 Separation Anxiety Disorder
andrew r. eisen and kristin l. toffey 550
20 Selective Mutism
christopher a. kearney, andrew gerthoffer, amanda
howard, and rachele diliberto 576

Published online by Cambridge University Press

 Contents ix

Section 5 Etiology and Phenomenology of Specific

OCD Spectrum Disorders 601
21 Obsessive-Compulsive and Related Disorders
lillian reuman and jonathan s. abramowitz 603
22 Body Dysmorphic Disorder
emma baldock and david veale 624
23 Hoarding Disorder
kristen s. springer, blaise l. worden, and david f. tolin 646
24 Body-Focused Repetitive Behavior Disorders
dan j. stein and christine lochner 669

Section 6 Etiology and Phenomenology of Specific

Trauma- and Stressor-Related Disorders 683
25 Acute Stress Disorder
joshua c. morganstein, suzanne yang, gary h. wynn,
david m. benedek, and robert j. ursano 685
26 Posttraumatic Stress Disorder
katherine buchholz, zoe feingold, and tara e. galovski 723
27 Reactive Attachment Disorder
kimberly renk 743

Section 7 Treatment and Prevention of Anxiety

and Related Disorders 769
28 Anxiety Disorders
joseph k. carpenter, kristina conroy, and stefan
g. hofmann 771
29 OCD Spectrum Disorders
martin e. franklin, simone budzyn, and holly freeman 805
30 Trauma- and Stressor-Related Disorders
andrew m. sherrill and sheila a. m. rauch 826
Index 863

Published online by Cambridge University Press

 Contributors

jonathan s. abramowitz, University of North Carolina at Chapel Hill,

Department of Psychology and Neuroscience
brian albanese, Florida State University, Department of Psychology
Nicholas Allan, Ohio University, Department of Psychology
Emma Baldock, King’s College London, Department of Psychology
miranda l. beltzer, University of Virginia, Department of Psychology
david m. benedek, Uniformed Services University, Department of Psychiatry
erin c. berenz, University of Illinois at Chicago, Department of Psychology
yannick boddez, University of Groningen, Department of Clinical Psychology
and Experimental Psychopathology, Katholieke Univeriteit (KU) Leuven, Center
for the Psychology of Learning and Experimental Psychopathology
katherine buchholz, National Center for PTSD
simone budzyn, University of Pennsylvania, School of Medicine
eric bui, Massachusetts General Hospital, Harvard Medical School
timothy a. brown, Boston University, Department of Psychology
rachel m. butler, Temple University, Department of Psychology
r. nicholas carleton, University of Regina, Department of Psychology
joseph k. carpenter, Boston University, Department of Psychology
peter j. castagna, Louisiana State University, Department of Psychology
kristina conroy, Boston University, Department of Psychology
kelly correa, University of Illinois at Chicago, Department of Psychology
rebecca cox, Department of Psychology, Vanderbilt University
thompson e. davis iii, Louisiana State University, Department of Psychology

Published online by Cambridge University Press

 List of Contributors xi

rachele diliberto, University of Nevada, Las Vegas, Department of

Psychology
andrew r. eisen, Fairleigh Dickinson University, School of Psychology
zoe feingold, National Center for PTSD
katya c. fernandez, Stanford University, Department of Psychology
martin e. franklin, University of Pennsylvania, School of Medicine
holly freeman, University of the Sciences in Philadelphia
tara e. galovski, National Center for PTSD
andrew gerthoffer, University of Nevada, Las Vegas, Department of
Psychology
fallon r. goodman, George Mason University, Department of Psychology
james j. gross, Stanford University, Department of Psychology
richard g. heimberg, Temple University, Department of Psychology
dirk hermans, Katholieke Univeriteit (KU) Leuven, Center for the Psychology
of Learning and Experimental Psychopathology
devon hinton, Massachusetts General Hospital, Harvard Medical School
stefan g. hofmann, Boston University, Department of Psychology
arielle horenstein, Temple University, Department of Psychology
amanda howard, University of Nevada at Las Vegas, Department of
Psychology
todd b. kashdan, George Mason University, Department of Psychology
christopher a. kearney, University of Nevada at Las Vegas, Department of
Psychology
andrew m. kiselica, University of South Florida, Department of Psychology
sarah e. kleiman, VA Boston Healthcare System
kelly a. knowles, Vanderbilt University, Department of Psychology
ernst h. w. koster, Ghent University, Department of Experimental Clinical and
Health Psychology
lucas s. lafreniere, Pennsylvania State University, Department of Psychology
maria a. larrazabal, George Mason University, Department of Psychology
daniel j. lee, National Center for PTSD, VA Boston Healthcare System, Boston
University School of Medicine

Published online by Cambridge University Press

 xii List of Contributors

carl lejuez, University of Kansas, Department of Psychology

wen li, Florida State University, Department of Psychology
christine lochner, Stellenbosch University, Department of Psychiatry
peter m. mcevoy, Curtin University, School of Psychology and Speech
Pathology, Centre for Clinical Interventions, Perth
joshua c. morganstein, Uniformed Services University, Department of
Psychiatry
amanda s. morrison, California State University at East Bay, Department of
Psychology
peter muris, Maastricht University, Department of Clinical Psychological
Science
marie nebel-schwalm, Illinois Wesleyan University, Department of
Psychology
michelle g. newman, Pennsylvania State University, Department of
Psychology
bunmi o. olatunji, Vanderbilt University, Department of Psychology
lance m. rappaport, Commonwealth University, Department of Psychology
sheila a. m. rauch, Emory University, Department of Psychiatry and
Behavioral Sciences
kimberly renk, University of Central Florida, Department of Psychology
lillian reuman, University of North Carolina at Chapel Hill, Department of
Psychology and Neuroscience
roxann roberson-nay, Commonwealth University, Department of
Psychology
anthony j. rosellini, Boston University, Department of Psychological and
Brain Sciences
sara scheveneels, Katholieke Univeriteit (KU) Leuven, Center for the
Psychology of Learning and Experimental Psychopathology
norman b. schmidt, Florida State University, Department of Psychology
stewart a. shankman, University of Illinois at Chicago, Department of
Psychology
andrew m. sherrill, Emory University, School of Medicine
sarah shihata, Curtin University, School of Psychology and Speech Pathology

Published online by Cambridge University Press

 List of Contributors xiii

ki eun shin, Pennsylvania State University, Department of Psychology

nicole short, Florida State University, Department of Psychology
kristen s. springer, The Institute of Living
ian stanley, Florida State University, Department of Psychology
dan j. stein, University of Cape Town, Department of Psychiatry and Mental
Health
eric a. storch, University of South Florida, Department of Psychology, Rogers
Behavioral Health – Tampa Bay, Johns Hopkins All Children’s Hospital
bethany a. teachman, University of Virginia, Department of Psychology
kristin l. toffey, Fairleigh Dickinson University, School of Psychology
david f. tolin, The Institute of Living, Yale University School of Medicine
esther s. tung, Boston University, Department of Psychology
robert j. ursano, Uniformed Services University, Department of Psychiatry
anouk vanden bogaerde, Ghent University, Department of Experimental
Clinical and Health Psychology
david veale, King’s College London, Department of Psychology
david watson, University of Notre Dame, Department of Psychology
frank w. weathers, Auburn University, Department of Psychology
alexandra j. werntz, University of Virginia, Department of Psychology
john t. west, George Mason University, Department of Psychology
blaise l. worden, The Institute of Living
gary h. wynn, Uniformed Services University, Department of Psychiatry
suzanne yang, Uniformed Services University, Department of Psychiatry;
Henry M. Jackson Foundation for the Advancement of Military Medicine

Published online by Cambridge University Press

Published online by Cambridge University Press
 Anxiety and Related Disorders
An Introduction

Rebecca C. Cox and Bunmi O. Olatunji

Anxiety disorders are characterized by fear and distress in the absence of objective
threat and are accompanied by physiological, cognitive, and affective symptoms.
Such fear and distress can occur in both anticipatory forms, as generalized anxiety
disorder (GAD), and in acute forms, as in panic disorder. With one-year and
lifetime prevalence rates of 18.1% and 28.8%, respectively (Kessler, Chiu,
Demler, & Walters, 2005a; Kessler et al., 2005b), anxiety disorders are one of the
most common psychiatric conditions.
Given the high prevalence of anxiety disorders, it is important to consider
their associated disability. Indeed, anxiety disorders are ranked as the sixth
leading cause of disability in both high- and low-income countries (Baxter,
Vos, Scott, Ferrari, & Whiteford, 2010) and are experienced as equally dis-
abling as many chronic physical conditions (Stein et al., 2005). Such deficits
can include problems with social relationships, responsibilities, and self-care
among adults (Hendriks et al., 2014) and diminished academic performance in
children and adolescents (Nail et al., 2015). Likewise, anxiety disorders are
associated with decreased quality of life (Mendlowicz & Stein, 2000). Notably,
quality of life is also impaired in subthreshold samples (Mendlowicz & Stein,
2000), suggesting that anxiety-related dysfunction is not limited to those with
the most severe disorders. Given such high levels of impairment, it is perhaps
unsurprising that anxiety disorders are costly. Anxiety disorders-related dis-
ability is associated with an economic burden ranging from $42.3 billion to
$46.6 billion annually (Greenberg et al., 1999; Rice & Miller 1998), making
anxiety disorders some of the costliest psychiatric conditions (Rice & Miller,
1998).
Despite the high prevalence and associated disability, much remains unknown
about the etiology and maintenance of anxiety and related disorders. What is
known is that anxiety disorders may be distinguished in part from other forms of
psychopathology by the typical age of onset. Indeed, anxiety disorders onset
relatively early (median age of onset = 11 years; Kessler et al., 2005b) and are
highly prevalent among children (Costello, Mustillo, Erkanli, Keeler, & Angold,
2003). Although childhood and adolescence appear to represent an important risk
window for the development of anxiety symptoms and disorders, researchers
continue to struggle to operationalize a comprehensive model that can fully account
for this sensitive period.

[Link] Published online by Cambridge University Press

 2 REBECCA C . COX AND BUNMI O . OLATUNJI

Research does suggest that treatment for anxiety disorders is often not sought
until adulthood (Christiana et al., 2000), indicating several years of untreated
symptoms in many individuals with these disorders. This delay between typical
age of onset and treatment may contribute to findings that suggest anxiety disorders
are generally chronic (Bruce et al., 2005). Prospective research indicates that the
majority of anxiety disorders persist over 12 years, with a lower probability of
recovery compared to major depressive disorder (Bruce et al., 2005). Recurrence is
also highly likely (Scholten et al., 2013), particularly among those with comorbid
conditions (Bruce et al., 2005). Further, daily functioning remains diminished in
those who remit from an anxiety disorder compared to controls (Iancu et al., 2014).
This is notable, given that functional impairment, along with anxiety sensitivity,
predicts anxiety disorder recurrence (Scholten et al., 2013).
Anxiety disorders are further complicated by high rates of comorbidity, as
approximately 90% of those with an anxiety disorder have a history of additional
psychopathology (Kaufman & Charney, 2000. Indeed, half of those with one
anxiety disorder meet criteria for another (Kaufman & Charney, 2000). Further,
anxiety disorders commonly co-occur with other psychological conditions, includ-
ing mood disorders, substance use disorders (Kessler et al., 2005a), and eating
disorders (Kaye, Bulik, Thornton, Barbarich, & Masters, 2004). Notably, anxiety
disorders often precede the development of these disorders (Goodwin & Stein,
2013; Rojo-Moreno et al., 2015; Wittchen, Kessler, Pfister, & Lieb, 2000), suggest-
ing that treating the anxiety disorder may result in improvement in the comorbid
condition.
Anxiety disorders also often co-occur with medical conditions. Indeed, anxiety
disorders are uniquely associated with medical disorders over and above the effects
of mood and substance use disorders (Sareen, Cox, Clara, & Asmundson, 2005a),
and this pattern of comorbidity is associated with increased illness severity (Katon,
Lin, & Kroenke, 2007). Though anxiety disorders co-occur with a wide range of
medical conditions, illnesses characterized by pain are particularly common in
those with an anxiety disorder (Harter, Conway, & Merikangas, 2003; Sareen et al.,
2005a). Further, reductions in health-related anxiety are associated with improve-
ments in pain conditions (McCracken, Gross, & Eccleston, 2002; Spinhoven, Van
der Does, Van Dijk, & Van Rood, 2010), suggesting the utility of targeting anxiety
comorbid with medical conditions.
Furthering our understanding of anxiety and related disorders can also save lives,
as anxiety disorders are linked to suicidal ideation and attempts, even after adjust-
ing for psychiatric comorbidity, in both cross-sectional (Cougle, Keough, Riccardi,
& Sachs-Ericsson, 2008; Nepon, Belik, Bolton, & Sareen, 2010; Sareen et al.,
2005b) and longitudinal samples (Sareen et al., 2005b). Further, one study found
that among individuals with a history of suicidality, 70% met criteria for an anxiety
disorder (Nepon et al., 2010). A similar relationship is also evident among adoles-
cents with anxiety disorders, with increased rates of suicide associated with
increased number of anxiety disorders (Boden, Fergusson, & Horwood, 2007).
Although the available literature clearly shows that a preexisting anxiety disorder is

[Link] Published online by Cambridge University Press

 Introduction 3

an independent risk factor for suicidality and that comorbid anxiety amplifies the
risk of suicide attempts among those with mood disorders, the psychobiological
processes that may explain this effect remain unclear.
Current understanding of the psychobiological processes associated with anxiety
has resulted in significant changes in the diagnostic classification of anxiety dis-
orders in recent years. In the modern classification system, the Diagnostic and
Statistical Manual of Mental Disorders (DSM), classes of disorders are clustered
around shared phenomenological features, with the defining features of anxiety
disorders being symptoms of anxiety and avoidance behavior (APA, 1987). Since
the introduction of diagnostic classes in DSM-III (APA, 1980), the anxiety dis-
orders class has consistently included panic disorder with/without agoraphobia,
specific phobias, social phobia, GAD, obsessive-compulsive disorder (OCD), and
posttraumatic stress disorder (PTSD). However, DSM-5 has represented a notable
departure from this standard, such that OCD and PTSD have been removed from
the anxiety disorders and placed within two newly created classes, obsessive-
compulsive and related disorders and trauma- and stressor-related disorders,
respectively (APA, 2013).
These changes have proved controversial. The obsessive-compulsive and
related disorders class was introduced on the assertion that OCD is phenom-
enologically and biologically distinct from anxiety disorders (Stein et al.,
2010). For example, proponents of the obsessive-compulsive and related dis-
orders class suggest that the distinguishing phenomenon of OCD is not anxiety,
but repetitive behaviors and emphasize the unique neural profile of hyperactiv-
ity in the fronto-striatal loop in OCD (Stein et al., 2010). In contrast, critics of
this approach argue that the one of the primary features of OCD is anxiety in
response to obsessions and that efforts to adapt classification systems based on
findings from neuroimaging research are premature (Abramowitz & Jacoby,
2014). Likewise, while proponents of the changes to PTSD in DSM-5 have
praised the addition of symptoms to the diagnostic criteria (Kilpatrick, 2013),
others have argued that the new criteria result in excessive heterogeneity
(Galatzer-Levy & Bryant, 2013).
Such controversies highlight the limitations inherent to categorical diagnostic
approaches. The utility of the diagnostic criteria defined by the DSM is to guide
differential diagnosis and selection of treatment and provide a common language
for practitioners (APA, 2013). Though the categorical diagnoses contained in the
DSM framework arguably imply true distinctions between disorders that represent
unique etiologies, DSM-5 notes that such a classification system may not fully
account for the various complexities of mental illness (APA, 2013). Indeed, critics
of the categorical approach have argued that the excessive rates of comorbidity
suggest shared etiology among multiple disorders that the categorical approach
would classify as distinct (Widiger & Samuel, 2005). For example, high comor-
bidity between GAD and depression may reflect shared genetic diatheses and
overlap of core phenotypic processes, such as negative affect (Mineka, Watson,
& Clark, 1998).

[Link] Published online by Cambridge University Press

 4 REBECCA C . COX AND BUNMI O . OLATUNJI

Likewise, the necessity of “black-and-white” boundaries between disorders in

a categorical system has contributed to a proliferation of new disorders designed to
bridge the gap between extant disorders, a practice that may reflect artificial cutoffs
of dimensional domains (Widiger & Samuel, 2005). This practice is seen in the
addition of acute stress disorder to DSM-IV to identify pathological stress
responses that surpass adjustment disorder but do not meet the minimum duration
required for PTSD (Marshall, Spitzer, & Liebowitz, 1999). In contrast,
a dimensional framework is arguably a better representation of complex pheno-
types that are unlikely to derive from singular etiologies. In addition to addressing
the issues of comorbidity and arbitrary distinctions, a dimensional framework also
allows for quantitative descriptions of severity and treatment progress and lends
itself to empirical elucidation of physiological underpinnings of observable symp-
toms (Helzer, Kraemer, & Krueger, 2006).
Research has shown that the severity, duration of anxiety, and disability are able
to better identify severe chronic course trajectory as compared with DSM-IV
categories (Batelaan, Rhebergen, Spinhoven, Van Balkom, & Penninx, 2014).
Findings of this sort suggest that a targeted focus on cross-cutting dimensions
may explain more variance in anxiety-related processes than diagnostic categories.
The purported benefits of such a dimensional approach to psychopathology has led
in part to the development of the National Institute of Mental Health (NIH)
Research Domain Criteria (RDoC). The RDoC outlines a framework in which
five core domains relevant for psychopathology (Negative Valence Systems,
Positive Valence Systems, Cognitive Systems, Social Processes, Arousal and
Regulatory Systems) can be measured and described at multiple levels ranging
from genes to self-report (Insel et al., 2010). RDoC represents a major departure
from the categorical diagnoses of the DSM in a push toward defining mental illness
by dysfunction along transdiagnostic dimensions. Importantly, in addition to taking
a step toward a dimensional diagnostic system, RDoC also asserts that mental
illnesses are “brain disorders” that can be understood and measured in terms of
dysfunction at genetic and molecular levels (Insel et al., 2010).
The RDoC perspective has been highly debated, particularly among cognitive
and behaviorally oriented psychological scientists (Deacon, 2013). The veracity of
this perspective remains to be seen, as clinical neuroscience is in its relative
infancy. Likewise, the RDoC’s impact on the future of anxiety and related disorders
research is unclear. Though neurobiology has been critical for delineating certain
mechanisms of anxiety-related pathology, such as fear conditioning (Lissek, 2012),
there is concern that behavioral or verbal indices are undervalued in a brain
disorders framework. Given that an important goal of the RDoC approach is to
inform the development of novel, circuit-based interventions and the personaliza-
tion of treatments available, it will be vital to examine the extent to which this
approach complements existing empirically supported models of anxiety and
related disorders.
Treatments of anxiety and related disorders have largely centered on two mod-
alities: psychotropic medications and cognitive behavior therapy (CBT). While

[Link] Published online by Cambridge University Press

 Introduction 5

a variety of psychotropic medications have been utilized for the treatment of

anxiety and related disorders, selective serotonin reuptake inhibitors (SSRIs) and
serotonin-norepinephrine reuptake inhibitors (SNRIs) are the current first-line
pharmacological agents due to both efficacy and tolerability (Ravindran & Stein,
2010). CBT for anxiety and related disorders generally includes intervention
strategies aimed at reducing maladaptive beliefs (e.g., cognitive restructuring)
and behavioral avoidance (e.g., exposure) (Hofmann & Smits, 2008).
Considerable research has found CBT to be efficacious for the treatment of anxiety
and related disorders (Hofmann & Smits, 2008; Olatunji, Cisler, & Deacon, 2010).
Extant research comparing CBT to psychotropic medications indicates comparable
efficacy, while evidence for an additive effect of combination treatments (i.e., CBT
+ medication) is mixed (Bandelow, Seidler-Brandler, Becker, Wedekind, & Ruther,
2007). However, CBT treatment gains are generally sustained over one to two years
(Butler, Chapman, Forman, & Beck, 2006), whereas medication effects are gen-
erally lost upon discontinuation (see Otto, Smits, & Reese, 2005, for a review).
Despite the established efficacy of CBT, a substantial proportion of patients do not
respond to CBT or relapse, and a paucity of research examines outcomes beyond
two years (Arch & Craske, 2009). These findings highlight major areas for
improvement to the current “gold standard” of psychotherapy. Paradigm shifts in
research, such as the dimensional approach and emphasis on neurobiology
espoused by RDoC, may yield novel treatment targets or personalized medicine
insights to increase treatment efficacy and decrease nonresponse and relapse.

Overview of This Book

Much remains unknown about the etiology, maintenance, and treatment of
anxiety and related disorders. This volume aims to bridge this gap in knowledge
with a focus on the divide between current classification systems and approaches to
anxiety and related disorders in a rapidly changing field. This book integrates many
levels of information to better explain the basic dimensions of functioning under-
lying anxiety and related disorders. First, Section 1 outlines basic mechanisms of
anxiety. Consistent with a dimensional perspective, Section 1 describes the effects
of basic processes of learning, perception, and attention on fear and anxiety. For
example, how might learning mechanisms that underlie fear conditioning contri-
bute to clinical fear and anxiety? Can the threat processing that underlies anxiety
and its disorders be modeled at the level of sensory perception? Consistent with the
RDoC research framework, Section 1 examines basic dimensions of functioning
that span the full range of human behavior from normal to abnormal. Section 2 then
describes various transdiagnostic processes that may confer risk for the develop-
ment of anxiety and related disorders. Transdiagnostic processes reflect common
psychological processes that underlie clinical syndromes. Section 2 highlights that
rather than focusing on discrete diagnostic entities, the co-occurrence of many

[Link] Published online by Cambridge University Press

 6 REBECCA C . COX AND BUNMI O . OLATUNJI

diagnoses likely reflects different patterns of symptoms that result from shared risk
factors and the same underlying processes.
Section 3 of this volume covers assessment, diagnosis, and cultural manifesta-
tions of anxiety and related disorders. DSM-5 represents a significant departure in
traditional conceptualizations of disorders that fall in the anxiety disorder category.
Section 3 highlights these changes as well as their implications for research and
practice. Sections 4–6 discuss the etiology and phenomenology of specific anxiety
disorders, OCD spectrum disorders, and trauma- and stressor-related disorders.
A common theme for Sections 4–6 is a critical analysis of contemporary models of
the development of the various disorders that is informed by basic science.
Furthermore, this part of the volume examines the potential implications for the
RDoC research framework in advancing current knowledge regarding the etiology
of anxiety and related disorders. Last, Section 7 examines the treatment and
prevention of anxiety and related disorders. This portion of the volume identifies
which treatments are most effective for anxiety and related disorders and why.
In addition to a survey of existing descriptive and experimental approaches to the
study of anxiety and related disorders, an important goal of this book is empirically
guided suggestions for the treatment of anxiety and related disorders.

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 SE C TI ON 1

Basic Mechanisms in Fear

and Anxiety

Published online by Cambridge University Press

Published online by Cambridge University Press
 1 Learning Mechanisms in Fear
and Anxiety
It Is Still Not What You Thought It Was
Sara Scheveneels, Yannick Boddez, and Dirk Hermans

Alex is a 24-year-old male who recently dropped out of work because it became
difficult to function well in his job as a communication assistant. For example,
he avoids making telephone calls in the presence of others and dodges having
lunch with his colleagues. When talking to a superior in particular, Alex is
extremely self-conscious and aware of certain physical symptoms such as blush-
ing, sweating, and trembling. He is afraid that others will notice these symptoms
and would evaluate him as incompetent, stupid, or weird. Alex grew up in
a family of lawyers in which the importance of a professional career was
stressed. Alex mentions that he has always been timid, but his social anxiety
became worse at university, especially after he gave a wrong answer on
a question during class. The professor reacted by saying that Alex did not
belong at university if he could not answer so obvious a question. Alex
responded to this by running out of the classroom. He remembers that his
classmates were laughing when he left, but he is not sure whether this memory
is accurate or he imagined it. After this incident, Alex started to skip classes and
avoided contact with his classmates.

Learning experiences play a crucial role in the etiology of anxiety. An individual

with social anxiety, such as Alex, might have learned that (saying something stupid
in) the company of others is related to rejection and exclusion, which might have
caused his current symptoms of social anxiety and avoidance. Learning theory has
not only provided valuable insights into the onset of anxiety disorders, it has also
given and still does give a major impetus in the development and optimization of
the treatment of anxiety.
In this chapter, we discuss how learning mechanisms as investigated in basic fear
conditioning research are at work in clinical fear and anxiety. We mainly examine
research in human (healthy and anxious) participants and occasionally address
findings from rodent research as well. The first section of this chapter focuses on
different procedures and outcomes when modeling fear acquisition in the labora-
tory. Subsequently, we evaluate whether we can translate the findings from fear
conditioning research in the laboratory to clinical anxiety based on three estab-
lished criteria of external validity: face validity, construct validity, and predictive
validity. We demonstrate that recent developments in the field can respond to often-
heard critiques on the classical fear conditioning model of anxiety.

13

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 14 SARA SCHEVENEELS , YANNICK BODDEZ , AND DIRK HERMANS

A Learning Perspective on the Etiology of Anxiety Disorders

A Classical Conditioning Account of Anxiety

One of the first, and without doubt most famous, case studies illustrating that fear
reactions can be acquired by learning experiences is the one of Albert B. as
described by Watson and Rayner (1920). A phobic reaction was induced in
Albert by pairing a stimulus that initially did not evoke fear (i.e., a white rat)
with an aversive outcome (i.e., a loud noise). After repeatedly seeing the rat
together with hearing the loud noise, Albert started to react fearfully to the rat.
This is one of the first demonstrations of fear conditioning, nowadays an estab-
lished procedure to induce fear in the laboratory.
Watson and Rayner’s early demonstration that anxiety for a stimulus can develop
by learning experiences, and in particular by pairing the stimulus with an aversive
event, relies on the experimental work of Pavlov (1927). Using dogs as subjects,
Pavlov paired stimuli such as sounds with food intake. Pavlov demonstrated that
the dogs initially did not show increased saliva production in response to the sound.
However, after several pairings of the sound together with the food, the sound
started to elicit increased saliva production. This is referred to as classical or
Pavlovian conditioning. We now use Pavlov’s procedure to define the concepts
involved in learning. The increased saliva production in response to the sound is
called the conditional response (CR). A CR can be defined as a change in respond-
ing that is conditional upon the relation between the presence of at least two stimuli
(De Houwer, Barnes-Holmes, & Moors, 2013). In Pavlov’s procedure, one of these
two stimuli is the sound, which functions as a conditional stimulus (CS). Such CS
can be defined as a stimulus to which responding changes conditional upon
a relation with another stimulus (i.e., with the food). The food stimulus itself is
termed the unconditional stimulus (US). In case of successful conditioning, the
US changes responding to the stimulus it is related to (i.e., to the CS).1 Notably, in
Pavlov’s early experiments, the US was an appetitive stimulus (i.e., food). This is
different for fear conditioning research, where the US is an aversive stimulus (e.g.,
loud noise). However, as becomes clear in the next paragraph, besides this, the
procedure is fairly similar.

(Human) Fear Conditioning: Procedures and Outcomes

The fear conditioning model is widely recognized as a model for the pathogenesis
of fear and anxiety disorders (e.g., Beckers, Krypotos, Boddez, Effting, & Kindt,
2013). Typically, the CS is paired (repeatedly) with an aversive US until it elicits
conditional responding indicative of fear and anxiety.
In human fear conditioning, a variety of stimuli has been used as a CS, ranging
from fairly neutral stimuli (e.g., geometrical shapes) to fear-relevant stimuli (e.g.,
spiders, fearful faces). Often the CS is a visual stimulus, but other modalities such
as auditory and olfactory stimuli have been used as well. An electrocutaneous

[Link] Published online by Cambridge University Press

 Learning Mechanisms in Fear and Anxiety 15

stimulus or electric shock is typically used in the laboratory as a US, with an

intensity set at a level that is perceived as “uncomfortable, but not painful” by the
individual participant. However, also auditory stimuli such as human screams or
(bursts of a) loud (white) noise (100–105 dB) and aversive pictures or movie clips
have been used as a US (e.g., Joos, Vansteenwegen, & Hermans, 2012; Lenaert
et al., 2014). For modeling panic symptoms in the laboratory, CO2-enriched
air leading to a sensation of breathing restriction has proven successful (Leibold
et al., 2013).
As described earlier, after pairing a CS (repeatedly) with a US, presenting the CS
will elicit a CR indicative of fear or anxiety. Several dependent variables can be
included as indices of fear and anxiety in response to the CS. In line with Lang’s
bio-informational theory (1979) and emotion theory (Frijda, 1986), dependent
variables in fear conditioning research can focus on each of the three response
systems: the verbal, psychophysiological, and behavioral levels.
On the verbal level, US expectancy ratings are commonly used by asking
participants to indicate the extent to which they expect US occurrence (Boddez
et al., 2013). In the example of Alex, this could correspond to the extent to which he
expects that others will exclude or reject him after saying something (stupid) during
lunchbreak. In addition to US expectancy ratings, ratings of subjective fear, CS
valence, and subjective units of distress are sometimes included.
As physiological indices, skin-conductance response (SCR) and fear-potentiated
startle (FPS) have a long history in human fear conditioning research. In SCR (also
known as galvanic skin response, electrodermal responding, or sympathetic skin
response), changes in the electrical conductance of the skin are measured. This is
informative for fear learning because the conductive properties of the skin are
influenced by sympathetic autonomic arousal and are reactive to signals of salient
events. Notably, SCR is not specific for the anticipation of aversive events, but
increases in response to any salient event (e.g., also appetitive ones) (Lipp, 2006).
In contrast to SCR, a potential advantage of FPS is that it is modulated by emotional
valence (Grillon & Baas, 2003, but see Mallan, Sax, & Lipp, 2009). For measuring
FPS in humans, an eye-blink reflex is elicited by the administration of a high-
intensity probe of white noise (e.g., Blumenthal et al., 2005). The amplitude of this
eye-blink reflex, as measured by the electromyographic activity of the muscles
around the eye (orbicularis oculi), is potentiated in anticipation of aversive events.
In addition to SCR and FPS, other physiological indices of fear and anxiety, such as
heart rate and pupil dilation, have been included in human fear conditioning studies
(e.g., Leuchs, Schneider, Czisch, & Spoormaker, 2017). Importantly, these phy-
siological indices correspond to the physical symptoms in clinical anxiety. In the
clinical example, Alex started to sweat when he was confronted with a fear-
eliciting situation such as when talking to a superior, typically resulting in
increased electrical conduction of the skin. In addition, his heart started pounding
really fast. He also reported that, while at the office, he had a tendency to startle
each time the telephone of a colleague rang.

[Link] Published online by Cambridge University Press

 16 SARA SCHEVENEELS , YANNICK BODDEZ , AND DIRK HERMANS

A third set of dependent variables is situated on the overt behavioral level.

As a key characteristic and one of the diagnostic criteria of anxiety disorders
(American Psychiatric Association, 2013), avoidance behavior can be considered
an indispensable outcome measure when modeling pathological anxiety. Alex’s
avoidance behavior was debilitating and prevented him from doing his job appro-
priately. Because he was afraid of saying something stupid or making a bad
impression, he avoided making telephone calls in the presence of colleagues,
going to team meetings, and having lunch with colleagues or superiors.
Nevertheless, whereas in most fear conditioning studies typically at least one
physiological and one verbal measure are included for reasons of convergent
validity, only a few research groups consistently include the assessment of avoid-
ance (tendencies) (Beckers et al., 2013). In fear conditioning research, avoidance
can be measured by giving participants the option to avoid the CS (e.g., Grillon
et al., 2006) or to avoid the US when presented with the CS (e.g., Van Meurs,
Wiggert, Wicker, & Lissek, 2014). Moreover, the avoidance response can vary in
cost, ranging from button presses to avoid the US without additional response cost
(Lovibond, Mitchell, Minard, Brady, & Menzies, 2009; Vervliet & Indekeu, 2015)
to avoidance responses associated with a cost, for instance a loss in points (Pittig,
Brand, Pawlikowski, & Alpers, 2014). In addition, visual avoidance (e.g., looking
away) can be assessed by using eye-tracking methodology (e.g., Rinck & Becker,
2006). Some studies include a separate approach-avoidance task to assess avoid-
ance tendencies or the urge to avoid (e.g., Krypotos, Arnaudova, Effting, Kindt, &
Beckers, 2015; Krypotos, Effting, Arnaudova, Kindt, & Beckers, 2014; Van Gucht,
Vansteenwegen, Van den Bergh, & Beckers, 2008). In such a task, a manikin figure
typically appears at the bottom or top of the screen and the CS is presented in the
opposite half of the screen. Participants are instructed to move the manikin toward
(approach) or away from (avoidance) the CS as quickly as possible by pressing
a key or by handling a joystick. The time between the CS onset and the response is
measured. If participants are faster to move the manikin away from the CS than
toward it, a tendency to avoid the CS is inferred.
For reasons of cross-validation, fear conditioning studies typically include more
than one dependent variable, usually a verbal measure and one or more psycho-
physiological measures. Importantly, correlations between outcome measures
often have shown to be only weak (e.g., Hodgson & Rachman, 1974). This
observed divergence in outcome measures can, apart from measurement error,
also be explained by the fact that the three response systems indeed represent
different and partly independent dimensions of fear and anxiety (Beckers et al.,
2013).
An important question is whether (human) fear conditioning can indeed serve as
a model for clinical anxiety disorders. As we discussed in the previous paragraph,
at a procedural level and with regard to outcome measures the fear conditioning
model shows some clear similarities with the pathogenesis and symptomatology of
clinical anxiety. In the next paragraph, we evaluate the validity of human fear
conditioning as a model for clinical anxiety disorders in a more systematic way.

[Link] Published online by Cambridge University Press

 Learning Mechanisms in Fear and Anxiety 17

The External Validity of the (Human) Fear Conditioning Model

It is considered one of the most important advantages of (human) fear conditioning
research that it allows modeling pathological behavior in healthy subjects. A main
assumption is that the knowledge and insights acquired through highly controlled
fear conditioning experiments can inform clinical practice. This assumption con-
cerns the external validity of the fear conditioning model. In the past, several
critiques have been formulated on this model, arguing that it might be too simplistic
to capture the complexity of clinical anxiety. Mineka and Zinbarg (2006) replied to
these critiques and illustrated how contemporary approaches of conditioning and
learning theory can overcome a substantial part of them. In what follows, we
elaborate on the work of Mineka and Zinbarg (2006) by providing a systematic
evaluation of the fear conditioning model using three established criteria of valid-
ity: face validity, construct validity, and predictive validity.2 These criteria have
been used to evaluate external validity in pharmacological and more recently in
behavioral research (Davey, 2017; Luyten, Vansteenwegen, van Kuyck, Gabriëls,
& Nuttin, 2011; Scheveneels, Boddez, Vervliet, & Hermans, 2016; Vervliet &
Raes, 2013).
Face validity. The most straightforward validity criterion is face validity. This
refers to the surface similarity between the (fear conditioning) model and the
(anxiety) disorder. As discussed in the previous section, at face value, the fear
conditioning model shows important similarities with clinical anxiety. Conditional
reactions that are observed in fear conditioning studies, such as SCR, startling, and
elevated heart rate, correspond to the physical reactions in real-life fear-eliciting
situations. In addition, a tendency to avoid the conditional stimulus as well as the
expectancy that the aversive outcome will occur can be observed in both fear
conditioning studies and clinical anxiety.
Notably, fear conditioning research in the laboratory typically uses simple,
unimodal stimuli such as geometrical shapes, whereas in real life, the learning
experiences often take place in more complex circumstances. Therefore, more
recently, the use of complex, multisensory stimulus configurations (e.g., audi-
tory, tactile, olfactory, visual) has been proposed to provide a better analogue
for real-life experiences (Waters, LeBeau, & Craske, 2017). Virtual and
augmented reality might be a useful technology to achieve this (e.g., Baas,
Nugent, Lissek, Pine, & Grillon, 2004). However, the added value of using
these more complex stimulus configurations still requires empirical testing.
More specifically, future research should reveal whether using more complex
stimulus configurations (as compared to simple stimuli) allows for better
translation to clinical anxiety with respect to, for example, newly proposed
treatment strategies.
Establishing and optimizing the face validity of the fear conditioning model can
be considered a first step, but it is not the most decisive criterion of external validity.
In the next paragraph, we continue with evaluating more significant criteria.

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 18 SARA SCHEVENEELS , YANNICK BODDEZ , AND DIRK HERMANS

Construct validity. The evaluation of the construct validity revolves around the
question whether the same (etiological) processes are at play in the model and the
clinical disorder. Different from face validity, construct validity is not about a first
impression, but about underlying mechanisms.
A first indication for similar (neurobiological) processes underlying the fear
conditioning model and clinical anxiety can be found in neuroimaging studies that
reveal a similar neurocircuitry involved in anxiety patients and in fear conditioning
in animals and healthy humans (e.g., Sehlmeyer et al., 2009). In particular, a central
role of amygdaloid nuclei has consistently been demonstrated in the acquisition and
expression of fear responses and across different anxiety disorders (e.g., Kent &
Rauch, 2003; Sehlmeyer et al., 2009; Shin & Liberzon, 2010). In addition, other
brain areas such as the hippocampus, insula, anterior cingulate cortex, and ven-
tromedial prefrontal cortex have been identified as regions of interest across
anxiety disorders and in fear conditioning research (e.g., Damsa, Kosel, &
Moussally, 2009; Etkin & Wager, 2007; Ipser, Singh, & Stein, 2013).3
An assumption of the conditioning approach is that learning processes underlie
the etiology and treatment of clinical anxiety. Early learning theorists such as
Watson used simple acquisition procedures to model the etiology of anxiety
disorders. In these procedures, one neutral stimulus (e.g., a white rat) was paired
with one aversive outcome (e.g., a loud noise). This simple acquisition procedure
has been subject to some important critiques. We discuss some of these earlier
shortcomings as well as how they are addressed by more recent developments in
learning theory.
A contemporary learning theory approach on the etiology of anxiety disorders.
One criticism that has been formulated on the conditioning perspective is that many
anxiety patients are not able to report a CS-US event that can account for the
current anxiety symptoms. A first possibility to nonetheless explain this from
a learning account is to simply assume that a CS-US event has occurred, but that
people are not accurate in remembering and retrospectively reporting this condi-
tioning experience (Merckelbach, Van den Hout, Hoekstra, & de Ruiter, 1989; Öst
& Hugdahl, 1981).
Alternatively and maybe more likely, generalization and higher-order condition-
ing might obscure learning as the actual cause of the anxiety symptoms.
Generalization is discussed in more detail later, but can already be illustrated by
an anecdote about Albert from the study by Watson and Rayner (1920). It was said
that Albert did not fear only white rats after the conditioning experience but also
women wearing fur coats. If Albert would have entered treatment with this
complaint, one might have speculated about the sensational (Freudian) origins of
this fear. Nonetheless, it can easily be explained by a learning account if one
assumes that the fear generalized from the rat to fur coats based on their looking
alike. With respect to higher-order conditioning, emetophobia (i.e., fear of vomit-
ing) may serve as an example. Although some dry foods (e.g., cereal without milk)
might never have been directly involved in an aversive learning experience, the

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 Learning Mechanisms in Fear and Anxiety 19

patient might relate these foods to difficulties to swallow, which in turn is related to
vomiting (Bouman & Van Hout, 2006). This allows for an explanation of fear and
avoidance of these foods from a learning perspective.
As discussed earlier, conditioning can be defined as a change in responding due
to a relation in the presence of stimuli (De Houwer et al., 2013). Importantly, this
definition also covers observational learning (e.g., Cameron, Roche, Schlund, &
Dymond, 2016). Take the example of a patient who developed dog phobia after
observing somebody else get bitten by a dog. Crucially, in such cases, the fear can
still be explained by (an observed) relation between the presence of stimuli; more
precisely, by a relation between the presence of a dog and a dog bite. In addition,
one might develop dog phobia if one is told that dogs cause bite wounds. In such
fear learning via instruction, the fear is caused by a verbal description of the
relation between the presence of stimuli. Accounting for learning via observation
and instruction of course significantly increases the explanatory territory of the
learning framework. Olsson and Phelps (2004) compared fear acquisition through
direct pairings, instructions, and observational learning in an experimental study
with human participants. In the Pavlovian (direct) learning group, a CS was paired
with an electric shock. The observational-learning group observed a confederate
that was presented with the CS paired with shock. Participants in the instructed-
learning group were given verbal instructions about the CS being followed by
shock. Interestingly, similar levels of conditional fear responding, as measured by
the skin-conductance response, were found for all three pathways. Moreover, in
follow-up studies, it has been demonstrated that the neural correlates of direct and
indirect pathways to fear acquisition are largely overlapping, with amygdala
activation observed in both pathways (Olsson, Nearing, & Phelps, 2007; Phelps,
Connor, Gatenby, Gore, & Davis, 2001). These results provide experimental
evidence that learning processes can be involved even when no direct conditioning
experience is reported by the patient (also see Rachman, 1977).
Another reason why patients may not be able to report a CS-US event that can
account for their anxiety symptoms is that USs may be more subtle than the bite of
an animal. For example, in patients suffering from chronic fatigue syndrome,
something as subtle as experiencing fatigue may function as a US. If such patients
learn a relation between stair climbing and fatigue, stair climbing may come to
elicit fear (Lenaert, Boddez, Vlaeyen, & Van Heugten, 2018). In the case of such
subtle USs, it is easy to overlook that learning is involved. A similar argument
holds for other interoceptive USs like panic (Bouton, Mineka, & Barlow, 2001).
Until now, we have discussed how learning theory can handle the observation
that many anxiety patients are not able to report a CS-US event that can account for
their anxiety symptoms. Another intriguing observation that learning theory has to
account for is that not everyone undergoing a traumatic event will eventually
develop an anxiety disorder (Poulton & Menzies, 2002). Although about 95% of
people experience one or more traumatic events during their lifetime, only 10–30%
develop an anxiety disorder (Engelhard, Van den Hout, & McNally, 2008). One can
make this insightful by assuming that additional variables also moderate the

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 20 SARA SCHEVENEELS , YANNICK BODDEZ , AND DIRK HERMANS

learning process. Such variables include temperamental/biological vulnerabilities

as well as interindividual differences in contextual/experiential factors before,
during, and following the conditioning experience. In the following paragraphs,
a selection of these variables is discussed. For a more comprehensive overview, we
refer the interested reader to Lonsdorf and Baas (2015) and Lonsdorf and Merz
(2017).
Given the same conditioning experience, some individuals are more vulner-
able to develop an anxiety disorder than others, due to moderation by indivi-
dual differences in genetic predisposition and temperamental factors. So far,
among the most established genetic factors identified as being related to
anxiety problems is a polymorphism in the serotonin transporter gene promoter
region, 5-HTTLPR4 (e.g., Lonsdorf & Kalisch, 2011). In particular, carriers of
the 5-HTTLPR s-allele have been found to suffer from more severe panic
symptoms and social anxiety (Lonsdorf et al., 2009; Miu, Vulturar, Chis,
Ungureanu, & Gross, 2013; but see Blaya, Salum, Lima, Leistner-Segal, &
Manfro, 2007). The 5-HTTLPR s-allele has been associated with anxiety-
related personality traits as well (Munafò et al., 2009). In addition, it has
been demonstrated consistently that the low-efficacy 5-HTTLPR s-allele is
associated with facilitated fear conditioning (e.g., Bauer, 2015; Lonsdorf
et al., 2009; Wendt et al., 2014). Importantly, in line with a diathesis-stress
model of psychopathology, the 5-HTTLPR genotype has been found to interact
with stressful life events. Klucken et al. (2013), for example, found that
carriers of the 5-HTTLPR s-allele showed elevated activity in the neural fear
network in response to a CS, but only if they had a history of stressful life
events.
In addition, particular personality traits might moderate the relation between
learning and anxiety. An extensive set of personality traits has been investigated in
this context. Among the most commonly studied measures is intolerance of
uncertainty (IU). Individuals scoring high on IU react negatively to uncertain
situations and consider such situations as threatening (e.g., Carleton, 2016;
Lonsdorf & Merz, 2017). Available evidence shows that IU is a transdiagnostic
risk factor for the development and maintenance of anxiety disorders (e.g., Gentes
& Ruscio, 2011; McEvoy & Mahoney, 2012). In some fear conditioning studies, IU
has been positively correlated with fear responding and generalization (e.g., Chin,
Nelson, Jackson, & Hajcak, 2016; Morriss, Macdonald, & Van Reekum, 2016;
Nelson, Weinberg, Pawluk, Gawlowska, & Proudfit, 2015). Notably, these results
were only observed under conditions in which the aversive US (i.e., an electric
shock) followed on 50% of the trials (Chin et al., 2016). These results confirm that
individuals high on IU show stronger fear responding in ambiguous situations.
Other studies, however, have failed to replicate these findings (e.g., Arnaudova
et al., 2013).
In addition, contextual factors before, during, or after the crucial conditioning
event can moderate its outcome by either protecting the individual against devel-
oping an anxiety disorder or by making the individual more vulnerable. Therefore,

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 Learning Mechanisms in Fear and Anxiety 21

it seems important to take into account the entire learning history when trying to
explain why some individuals do and some do not develop an anxiety disorder even
though experiencing the same trauma. We now demonstrate that these contextual
factors fall within the scope of learning theory as well.
If an individual has safe experiences with the CS prior to conditioning, this can
attenuate the development of a CR. For example, if a tone is first repeatedly
presented by itself and in a second phase presented together with electric shock,
then fear will develop slower as compared to when pre-exposure to the tone did
not happen. In learning theory, this phenomenon is referred to as latent inhibition
(Lubow & Moore, 1959). Similarly, it has been shown that nontraumatic experi-
ences with the event or stimulus prior to trauma (e.g., visiting the dentist) are
protective against the development of psychopathology (e.g., dental phobia)
(Kent, 1997). On the other hand, preexisting stress or trauma can make an
individual more vulnerable to developing an anxiety disorder following
a conditioning event. In a study by Rau, Decola, and Fanselow (2005), rats
were exposed to a very mild electric shock in a specific cage (say, cage B).
Importantly, the experimental group received 15 heavy shocks in a very different
cage in advance (say, cage A), whereas the control group did not undergo this
additional treatment. At test, rats in the experimental group behaved very fearful
in cage B (more so than rats in the control group), even though they had only
received a mild shock in this cage. This might serve to explain why post-
traumatic stress disorder (PTSD) patients or individuals with already increased
stress levels are more sensitive to develop new anxieties after a mild aversive
event. In the example of Alex, having bad experiences in social situations in the
past (e.g., being bullied as a child) could have made him more vulnerable to
develop social anxiety after the incident with the professor.
During conditioning or the traumatic event, having a sense of control or mastery
might be a protective factor. Mineka, Cook, and Miller (1984) presented one group
of rats with unsignaled escapable shocks and another group of yoked subjects with
the same amount of unsignaled but – crucially – inescapable shocks. The group that
could not escape the shocks showed more freezing to both the conditioning context
and cue than the group that could escape the shock. Similar results have been found
in humans by Meulders et al. (2013). Participants that had control over the offset of
the US showed less conditional responding than a group of participants that had no
such control. Almost immediately after Alex gave the wrong answer, he realized
that he had misunderstood the professor’s question. Alex could have felt more
control or mastery if he had replied to the professor’s nasty remark with a joke or
even with a simple statement that he had misunderstood the question. Instead, he
panicked and ran out of the room.
Finally, contextual variables after conditioning can moderate whether a
learning experience results in clinical anxiety. In learning theory, a phenom-
enon referred to as US inflation has been described: the isolated presentation of
a strong US after a conditioning experience with a mild US can result in an
increase in conditional fear responding (Rescorla, 1974). For example, having

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 22 SARA SCHEVENEELS , YANNICK BODDEZ , AND DIRK HERMANS

a severe panic attack after having experienced mild panic in an elevator

might strengthen fear responding to the elevator even if the severe panic
attack did not occur in the elevator. Importantly, the inflation effect can also
be installed by providing verbal information about the US (e.g., den
Hollander, Meulders, Jakobs, & Vlaeyen, 2015). For instance, an individual
can initially experience only limited driving anxiety and avoidance after
a car accident. However, verbal threat information about the potential con-
sequences of the accident by others afterward might increase fear responding
and avoidance. Similarly, Alex’s parents, attaching much importance to
a professional career, responded to the incident by saying that he will
definitely not be able to pursue a career at a university following such
a negative remark from the professor.
In addition, repeatedly thinking or ruminating about the traumatic event can
make an individual more vulnerable to develop an anxiety disorder.
In particular, worrying or ruminating about the conditioning experience might
result in repeated activation of the CS-US contingency, which might strengthen
and retain the fear memory. Joos, Vansteenwegen, and Hermans (2012) inves-
tigated this in a human fear conditioning study. In an acquisition phase,
participants learned two CS-US contingencies. Both CSs were pictures of
faces; the USs were a human scream and a burst of white noise. Participants
were instructed to rehearse one of these contingencies in an experimental
session and during the subsequent week. More precisely, they were asked to
“think back to the picture (CS), the scream/noise (US) and the relationship
between them.” When tested with both CSs one week after acquisition, it was
found that fear responding was better retained for the contingency that was
rehearsed than for the non-rehearsed contingency. Importantly, these results
could not be explained by merely rehearsing the CS or by increasing the
negative value of the US representation (i.e., US inflation; Davey &
Matchett, 1994). In a follow-up study by Joos, Vansteenwegen, Vervliet, and
Hermans (2013), rehearsal of the CS alone failed to produce sustained respond-
ing. Moreover, in Joos et al. (2013) two CSs were paired with the same US.
Whereas changes in the US representation would impact both CSs similarly, it
was found that only the CS from the rehearsed CS-US contingency resulted in
sustained responding. This indicates that the CS, the US, and the contingency
between them have to be rehearsed in order to obtain the effect. Taken
together, this set of experiments provides another explanation of why not
everyone undergoing a traumatic event will eventually develop an anxiety
disorder: rumination moderates the outcome of the learning process in such
a way that rumination increases the risk.
More complex procedures to model the acquisition of fear and anxiety. Early
learning theorists such as Watson used simple acquisition procedures, in which one
neutral stimulus was paired with one aversive outcome, to model the etiology of
anxiety disorders. This simple acquisition procedure has been subject to some
important critiques. In the previous section, we discussed how a learning

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 Learning Mechanisms in Fear and Anxiety 23

theoretical account can overcome this criticism and expand its explanatory territory
by including phenomena that moderate the learning process. In this section, we
introduce a set of complex learning procedures that further add to the construct
validity of the fear conditioning approach. More precisely, we discuss three
procedures that mimic important but underappreciated processes underlying anxi-
ety disorders: (1) context conditioning, (2) inhibitory conditioning, and (3)
generalization.5
In a typical context conditioning procedure, a CS is paired with a US (i.e., simple
acquisition procedure) in a control group, whereas the experimental group receives
USs that are presented explicitly unpaired with the CS (e.g., Grillon & Davis,
1997). As a result of these unpaired CS-US presentations, the context (rather than
a discrete CS) indicates that the US might occur somewhere in the not too distant
future. Note that context in these experiments is typically operationalized as
a background picture or color on the computer screen that stretches out in time
before and after CS and US presentation (although other operationalizations have
been used as well; Boddez et al., 2014). Context conditioning typically results in
a sense of unpredictability and in a generalized and sustained state of arousal,
because participants cannot precisely predict when the US will occur (e.g., Grillon,
2002; Grillon, Baas, Lissek, Smith, & Milstein, 2004).
Context conditioning has been proposed as a model for pathological conditions
that are characterized by chronic, future-oriented (anticipation) anxiety, such as
generalized anxiety disorder (e.g., Luyten, Vansteenwegen, Van Kuyck, & Nuttin,
2011). In addition, context conditioning might also explain agoraphobic avoidance
often observed in individuals with panic disorder (e.g., Craske, Glover, & DeCola,
1995; Gorman, Kent, Sullivan, & Coplan, 2000). In particular, un-cued panic
attacks might serve as USs that are not predicted by discrete cues but merely
occur in a particular context (e.g., a supermarket). As a consequence, people
might come to avoid the entire context and related contexts (e.g., crowded places),
engaging in generalized avoidance. Therefore, one component in the treatment of
panic disorder is to identify discrete exteroceptive and interoceptive cues that are
predictive for panic attacks (Craske & Barlow, 2008). Fonteyne, Vervliet, Baeyens,
and Vansteenwegen (2009) provided experimental evidence for the importance of
this treatment component. They used a context conditioning procedure in which
both groups received predictable shocks (i.e., paired with a discrete CS) in context
A and shocks that were presented unpaired with a discrete CS in context
B. As predicted, higher contextual fear was observed in context B as compared
to context A. To investigate whether increasing the predictability of the US would
reduce contextual fear, in a subsequent phase the shocks were signaled by a novel
discrete CS in context B. Results showed that this intervention led to a reduction of
contextual fear and therefore confirmed that increasing predictability can decrease
contextual fear.
A second set of complex conditioning procedures relates to discriminating
between danger and safety. In real life, the ability to discriminate between stimuli
that signal danger and stimuli that indicate the absence of danger can be considered

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 24 SARA SCHEVENEELS , YANNICK BODDEZ , AND DIRK HERMANS

highly adaptive. For instance, the symptoms of a panic attack might resemble a life-
threatening heart attack or a stroke, but are in fact innocuous (Haddad, Pritchett,
Lissek, & Lau, 2012). Responding to a panic attack as if it is a heart attack or
a stroke leads to unnecessary escape and avoidance and an inefficient use of
resources. The ability to discriminate between danger and safety cues can be
modeled in a differential inhibition procedure, in which one stimulus (CS+) is
paired with an aversive outcome, whereas another stimulus (CS−) predicts the
absence of an aversive outcome. Using this procedure, elevated fear responding to
safe stimuli (CS−) and impaired discrimination between danger and safety cues
have been found in individuals with subclinical levels of anxiety (e.g., Ganzendam,
Kamphuis, & Kindt, 2013; Haddad et al., 2012) and in patients with clinical anxiety
(Duits et al., 2015; Lenaert, Boddez, Vervliet, Schruers, & Hermans, 2015; Lissek
et al., 2005; Lissek et al., 2009). This suggests that the differential inhibition
procedure taps into a process that is relevant to anxiety disorders and therefore
has construct validity. Nonetheless, it should also be mentioned that some fear
conditioning studies failed to find an effect of trait anxiety or observed an effect in
only one of the outcome measures but not in the other(s) (e.g., Kindt & Soeter,
2014; Torrents-Rodas et al., 2013).
Other procedures have been used to examine impairments in safety learning.
One of them is the conditioned inhibition procedure, a procedure known from the
animal literature. In intermixed trials, one stimulus A is paired with the US, but
when this stimulus is presented together with another stimulus B, the US is omitted.
This procedure corresponds to the use of safety signals in clinical practice. For
example, an individual with driving phobia might be fearful of driving on
a highway (A), but feel safe when accompanied by a passenger (AB). Here as
well, it has been found that high-anxious individuals show higher fear responding
to the safe AB stimulus compound than low-anxious individuals (Chan &
Lovibond, 1996; Grillon & Ameli, 2001).
A third defining feature of anxiety disorders is stimulus generalization. Boddez,
Bennett, Van Esch, and Beckers (2017) proposed to speak of generalization when
a stimulus elicits a response due to a learning experience in which that stimulus as
such was not featured. As an example, consider a child experiencing painful skin
burns upon touching the stove in his grandparents’ place. Behaving cautious
around not just this but any stove will prevent the child from acquiring additional
skin burns. In anxiety disorders, however, fear responding typically spreads to
a range of stimuli and situations that are not dangerous (Dymond, Dunsmoor,
Vervliet, Roche, & Hermans, 2015; Hermans, Baeyens, & Vervliet, 2013).
An individual suffering from dog phobia, for instance, will typically not only
react with intense fear to the specific dog involved in the biting incident (who
has proven dangerous), but to each and every dog.
In perceptual stimulus generalization, the fear responding is elicited by stimuli
that share perceptual similarity with the original CS+ (Kalish, 1969; Lissek et al.,
2010). The person suffering from dog phobia can be considered an example of
perceptual generalization. In a fear conditioning paradigm, Lissek et al. (2008)

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 Learning Mechanisms in Fear and Anxiety 25

investigated perceptual generalization by presenting small- and large-sized circles

as CS+ and CS−, respectively, counterbalanced across participants. Subsequently,
perceptual generalization of fear responding was tested by presenting participants
with circles that ranged in size between the CS+ and CS− (i.e., generalization
stimuli). This generated a generalization gradient, with stronger fear responses to
stimuli that resemble the CS+ and decreasing responding with decreasing similar-
ity. Using this procedure, stronger responding to the generalization stimuli (GSs)
has been observed in patients with panic disorder (Lissek et al., 2010), generalized
anxiety disorder (Lissek et al., 2014), and posttraumatic stress disorder (Lissek &
Grillon, 2012) compared to healthy controls. Taken together, this suggests that the
generalization procedure seizes a mechanism that is relevant to anxiety disorders
and therefore is construct valid.
It is important to note that perceptual generalization can also involve interocep-
tive CSs (Dymond et al., 2015; Lissek et al., 2010; Schroijen & Pappens, 2015).
In a patient suffering from panic disorder, fear responding might be elicited not
only by the interoceptive symptoms that directly preceded and accompanied the
first panic attack (e.g., tight chest), but also by other physical symptoms (e.g., full
stomach after overeating).
In addition to these different forms of perceptual generalization, fear responses
can also generalize across stimuli that diverge greatly in perceptual features, based
on non-perceptual grounds such as categories and conceptual knowledge (e.g.,
Dunsmoor & Murphy, 2015). Alex not only avoided going to the class of the
specific professor that was involved in the incident, he also skipped other classes
and started to avoid all kinds of (social) situations, including going to activities of
the student club and meeting new people. Although these situations might clearly
differ from the original learning experience with regard to their physical character-
istics, they can be considered part of an idiosyncratic category of situations in
which Alex considers himself at risk of saying something stupid and being rejected
by others. This type of generalization is called non-perceptual-based generaliza-
tion (Dymond et al., 2015).
As an experimental illustration, Dunsmoor, Martin, and LaBar (2012) presented
participants with a heterogeneous collection of images of animals and tools. Images
of one of these categories (e.g., animals) served as the CS+ category and were
paired with an electric shock; the other stimulus category (e.g., tools) was never
reinforced (i.e., CS− category). Subsequently, they tested for the generalization of
fear to new stimuli stemming from the CS+ and CS− category. Results indicated
higher fear responding, as measured by shock expectancy and skin-conductance
response, to stimuli stemming from the CS+ category compared to stimuli from the
CS− category. These results suggest that fear can generalize based on categorical
and conceptual knowledge. However, this paradigm using stimuli from preexisting
categories does not allow ruling out the potential influence of perceptual similarity
on the generalization of fear. It can indeed be argued that all stimuli of one category
(e.g., animals) share more perceptual similarity with each other than with stimuli
from the other category (e.g., tools).

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 26 SARA SCHEVENEELS , YANNICK BODDEZ , AND DIRK HERMANS

To completely rule out the potential influence of perceptual overlap,

research has been conducted using de novo categories by inducing concept-
like relations between arbitrary stimuli in an experimental way. Vervoort,
Vervliet, Bennett, and Baeyens (2014) investigated the generalization of fear
acquisition within novel arbitrary categories by first creating two four-member
stimulus equivalence categories (i.e., A1-B1-C1-D1 and A2-B2-C2-D2). This
was done using a matching-to-sample task. Stimuli were arbitrary line draw-
ings. In the matching-to-sample task, a sample stimulus was presented
together with two comparison figures and participants were instructed to
choose the comparison figure that matched the sample stimulus. After every
trial participants received feedback on whether their response was correct.
Next, one member of the first category (B1) was presented repeatedly with an
electric shock, whereas the member of the second category (B2) was never
paired with a shock. In a subsequent test for generalization in which C1, D1,
C2, and D2 were presented, it was found that conditional fear responses
generalized to other members of the arbitrary category (i.e., C1, D1). These
results confirm that fears can generalize across conceptually related stimuli in
addition to perceptually related stimuli.
Finally, Boddez et al. (2012) used a blocking procedure to assess fear general-
ization. In the first stage of the experiment, a CS was paired with a US.
In a subsequent phase, a second CS was presented in compound with the first
CS. This compound was paired with the same US as in the first phase. The newly
added second CS therefore did not provide any information about the onset of the
US over and above the information provided by the first CS. Interestingly, high trait
anxious participants showed higher fear responding when this second CS was
presented by itself at test. Such deficit in blocking might explain why certain
individuals are more prone to develop clinical anxiety. A soldier might, for
example, have experienced a bomb attack preceded by different cues such as
a screaming colleague warning of the attack, a sandy surface, and the fire of the
bombing raid. A deficit in blocking would imply that the soldier, after his mission,
does not only experience anxiety when a colleague is warning of another bomb
attack (i.e., the most informative cue), but also when he is invited to a barbecue
(fire) or when visiting the beach (sand).
In summary, we discussed complex learning procedures that allow the mimick-
ing of specific processes at play in anxiety disorders. As such, these procedures add
to the construct validity of the fear conditioning approach.
Predictive validity. Arguments about theoretical processes notwithstanding,
an important question remains whether the fear conditioning model allows for
translation to real-life situations that pertain to clinical anxiety. This concerns
the predictive validity of the fear conditioning model and is discussed now.
Two aspects of predictive validity can be distinguished (Scheveneels et al.,
2016). A first aspect refers to whether environmental variables exert a similar
influence in the fear conditioning model and in real-life situations. A second
aspect concerns testing whether a factor at the level of the individual exerts

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 Learning Mechanisms in Fear and Anxiety 27

a similar influence as well. Both aspects are about the question of whether
a factor, be it an environmental intervention or at the level of the individual,
moderates the relation between learning experiences and fear in the lab in the
same way as the relation between aversive experiences and anxiety symptoms
in real life.
Do interventions have a similar effect in the fear conditioning model and in
real life? With regard to the first aspect of predictive validity, presenting the
CS without US following fear conditioning is known to result in a decrease in
fear responding (e.g., Hermans, Craske, Mineka, & Lovibond, 2006). This
procedure is termed fear extinction. Interestingly, in real life, a similar inter-
vention also results in a decrease in fear responding, thus adding to the
predictive validity of the fear conditioning account. Indeed, exposure therapy
or repeated and systematic confrontation with the feared stimulus or situation
without occurrence of the expected aversive outcome is the (psychological)
treatment of choice in anxiety (e.g., Cusack et al., 2016; Öst, Havnen, Hansen,
& Kvale, 2015, Wolitzky-Taylor, Horowitz, Powers, & Telch, 2008). During
treatment, Alex was exposed to those social situations in which he expected to
be rejected by others, such as making telephone calls when his colleagues are
in the same room, meeting new people at parties, and returning things to
shops After repeated confrontation with these situations, Alex reported experi-
encing less anxiety.
In addition, experimental research has demonstrated that fear responding can
return after (partial or complete) fear extinction (Rachman, 1989; Vervliet,
Craske, & Hermans, 2013). In clinical practice, a return in fear responding is
unfortunately not uncommon either. It is estimated that 19–62% of clients
experience at least some return of fear after exposure-based treatment (Craske
& Mystkowski, 2006). Interesting for our present purposes, the interventions that
cause a return of fear after extinction in experimental conditioning studies
correspond to pathways to return of fear in real life. This again confirms the
predictive validity of the model (Vervliet et al., 2013). We now discuss the most
well-studied pathways to return of fear: spontaneous recovery, (context) renewal,
and reinstatement.
In the laboratory, return of fear can occur when a time interval is intro-
duced after extinction. Pavlov (1927) described this phenomenon as sponta-
neous recovery, and it has been established in multiple laboratory studies
(e.g., Huff, Hernandez, Blanding, & LaBar, 2009; Norrholm et al., 2008).
Spontaneous recovery in the lab corresponds to the clinical observation that
due to the mere passage of time after exposure treatment, a client can show
a reappearance of fearful responding (e.g., Mystkowski, Craske, Echiverri, &
Labus, 2006; Vasey, Harbaugh, Buffington, Jones, & Fazio, 2012).
A second manipulation that causes return of fear and that has been investi-
gated in fear conditioning research is a change in (background) context between
extinction and a subsequent test phase. This is referred to as (contextual)
renewal (e.g., Bouton, 2002; Effting & Kindt, 2007; Vervliet, Baeyens, Van den

[Link] Published online by Cambridge University Press

 28 SARA SCHEVENEELS , YANNICK BODDEZ , AND DIRK HERMANS

Bergh, & Hermans, 2013). Typically, if CS-US pairings during acquisition take place in
context A and fear is extinguished in context B, return of fear responding is
observed if the CS is presented in the acquisition context A (ABA renewal) or
in a novel context C (ABC renewal) (Bouton & Bolles, 1979). In clinical practice,
this corresponds to a relapse after successful treatment when the feared object or
situation is encountered outside the treatment context. Mystkowski, Craske, and
Echiverri (2002) investigated return of fear after a context change in a sample of
spider-anxious individuals. All participants received a one-session exposure-
based therapy in which they were exposed to a spider in one particular context.
Fear responding to the spider was tested one week later in the treatment context as
well as in a novel context. Significantly higher fear responding was observed in
the novel context as compared to the treatment context. Importantly, also the
therapist can be considered as a contextual factor: being confronted with the
feared stimulus or situation in the absence of the therapist after (successful)
treatment can result in a return of fear responding (Rodriguez, Craske, Mineka,
& Hladek, 1999). Based on these findings, extinction in multiple contexts has been
shown to reduce renewal in the laboratory (e.g., Bandarian-Balooch, Neumann, &
Boschen, 2012). Similarly, exposing a patient to the feared stimulus in multiple
contexts during clinical treatment (e.g., in the treatment context, at home etc.) can
attenuate return of fear responding (e.g., Olatunji, Tomarken, Wentworth, &
Fritsche, 2017; Vansteenwegen, Vervliet, Hermans, Thewissen, & Eelen, 2007).
A third intervention to induce return of fear is reinstatement. This refers to a return
in fear responding due to unsignaled US presentations after extinction (Haaker,
Golkar, Hermans, & Lonsdorf, 2014; Hermans et al., 2005). Reinstatement can be
seen as the equivalent of a return of fear after unsignaled panic attacks or if the
previously feared stimulus is encountered after a stressful event or in a distressing
situation. After successful treatment, Alex experienced a short-term recurrence of
social anxiety after someone commented to him about his blushing face.
A similar argument can be made with regard to pharmacological interventions for
anxiety. If the fear conditioning model has predictive validity, a pharmacological
intervention that has been shown to effectively reduce clinical anxiety should exert
a similar effect in the fear conditioning model. Among the leading pharmacological
interventions for anxiety are benzodiazepines (e.g., Offidani, Guidi, Tomba, & Fava,
2013). In the fear conditioning model, there is evidence that contextual fear (but not
CS-specific fear) can be reduced by benzodiazepines such as alprazolam (Baas et al.,
2002; Grillon et al., 2006). These results suggest that more complex learning
procedures such as context conditioning are more useful to test the clinical utility
of anxiolytic interventions compared to the simple acquisition procedure.
Do factors at the level of the individual have a similar effect in the fear
conditioning model and in real life? This aspect of predictive validity concerns
testing whether a factor at the level of the individual moderates the relation between
learning experiences and fear in the lab in the same way as the relation between
learning experiences and anxiety in real life.

[Link] Published online by Cambridge University Press

 Learning Mechanisms in Fear and Anxiety 29

In a longitudinal design, Lenaert et al. (2014) tested whether generalization and

discrimination learning in a human fear conditioning procedure could predict
subclinical levels of anxiety at a six-month follow-up. A large sample of first-
year students completed a differential inhibition procedure followed by
a generalization test. US expectancy ratings were used as the outcome measure.
Lenaert et al. (2014) argue that first-year students are particularly interesting
because the transition to university is accompanied by a set of real-life aversive
experiences related to academics, finances, social interaction, and other issues.
Crucially, students who showed deficiencies in discriminating between the
CS+ and CS− in the differential inhibition procedure (i.e., impaired safety learning)
reported higher levels of anxiety at a six-month follow-up. In addition, elevated
responding to the generalization stimuli closer to the CS− predicted higher levels of
anxiety at follow-up. These findings suggest that these complex conditioning
procedures have predictive validity. More precisely, it seems that the way in
which characteristics of the individual affect the effect of aversive experiences
on fear expression is the same in the laboratory as in real life.
In other studies, soldiers and firemen were used as subjects. The logic underlying
these studies was the same: to assess whether individuals react similarly to aversive
learning experiences in the lab as they do in real life. Needless to say, soldiers and
firemen are confronted with a plethora of aversive learning experiences, making
this an interesting population. Sijbrandij, Engelhard, Lommen, Leer, and Baas
(2013) found that impaired safety learning in the lab was associated with PTSD
symptoms at two and nine months post deployment to Afghanistan. Similar find-
ings were reported by Lommen, Engelhard, Sijbrandij, Van den Hout, and Hermans
(2013) and by Acheson et al. (2015). Guthrie and Bryant (2006), in their turn, found
that deficits in extinction learning in the lab are a risk factor for PTSD symptoms
after trauma exposure in firemen.
In conclusion, performance in the fear conditioning model allows the prediction
of (sub)clinical levels of anxiety, pointing toward a key role for conditioning in
(clinical) anxiety. Importantly, this paves the way for targeted prevention in
individuals who are at higher risk.

Conclusion
Fear conditioning procedures have been applied extensively as a model for
the acquisition of (clinical) fears and anxiety. In this chapter, we described the fear
conditioning model and evaluated its external validity based on three validity
criteria: face validity, construct validity, and predictive validity. The fear condition-
ing model shows sufficient face validity and allows for further increasing of the
similarities between the fear conditioning model and clinical anxiety by including
technologies such as virtual reality. Some critiques have been formulated with
regard to whether the (etiological) processes that underlie the fear conditioning
model are the same as those at work in clinical anxiety (i.e., construct validity).

[Link] Published online by Cambridge University Press

 30 SARA SCHEVENEELS , YANNICK BODDEZ , AND DIRK HERMANS

In particular, the simple fear acquisition model, as proposed by Watson, might be

insufficient to explain why some individuals develop anxiety disorders and others
do not. We discussed how modern learning approaches have addressed these
criticisms by, among other things, taking into account contextual variables before,
during, or after the conditioning experience. Furthermore, the use of more complex
conditioning procedures might add to the construct validity of the fear conditioning
model by mimicking additional processes at play in anxiety disorders. In the
section on predictive validity, we discussed that environmental and individual-
level factors that decrease and increase fear after aversive experiences in the lab
also do so in real life. In conclusion, the fear conditioning approach allows the
investigation of the acquisition of fear under highly controlled circumstances and
makes it possible to identify the exact (learning) mechanisms involved in the
etiology of anxiety disorders. This knowledge can provide meaningful directions
in how to prevent and treat (clinical) anxiety.
This work was supported by KU Leuven Program Funding Grant PF/10/005
awarded to Dirk Hermans and by the Belgian Science Policy Office Grant P7/33.

Notes
1. Changes in responding to the US, as caused by its relation with the CS, are possible but are typically left
uninvestigated in conditioning research.
2. The reader may note that the subtitle of our chapter (“It is still not what you thought it was”) is similar to
the subtitle used in Mineka and Zinbarg’s (2006) article.
3. Results regarding these areas are less univocal and their role remains a subject of discussion (e.g.,
Maren, 2008; Sehlmeyer et al., 2009).
4. Importantly, the field of genetics in psychopathology is characterized by several pitfalls and limitations
such as small effects, post hoc testing, underpowered studies, and failed replications. We refer the
interested reader to Dick et al. (2015), Duncan and Keller (2011), and Tabor, Risch, and Myers (2002)
for a more elaborate discussion of this topic.
5. For a more elaborate review of complex conditioning procedures, we refer the interested reader to
Boddez, Baeyens, Hermans, and Beckers (2014).

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