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Article
A Transdiagnostic Perspective on
Cognitive, Affective, and Neurobiological
Processes Underlying Human Suffering
Research on Social Work Practice
2014, Vol 24(1) 142-151
ª The Author(s) 2013
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DOI: 10.1177/1049731513503909
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Eric L. Garland1 and Matthew O. Howard2
Abstract
The Diagnostic and Statistical Manual of Mental Disorders and International Classification of Diseases classify mental health
disorders on the basis of their putatively distinct symptom profiles. Although these nosologies are highly influential, they also have
been derided as mere ‘‘field guides’’ because they focus solely on the superficial symptomatic expression of psychiatric syndromes
rather than on the commonalities underlying psychiatric disorders. Recently, an alternative transdiagnostic perspective has
emerged. This review addresses transdiagnostic processes that underlie a wide range of psychosocial problems commonly
addressed by social work practitioners. First, we describe how the transdiagnostic perspective differs from categorical views of
psychopathology and accords more closely with scientific evidence. Next, we review current experimental psychopathology and
neuroscience research to detail the cognitive, affective, and neurobiological features of five transdiagnostic processes. Finally, we
discuss how the transdiagnostic perspective may improve therapeutic outcomes and guide the implementation of targeted social
work interventions.
Keywords
cognitive bias, information processing, psychopathology, suppression, transdiagnostic
Globally influential taxonomies, such as the Diagnostic and Statistical Manual of Mental Disorders (DSM) and International
Classification of Diseases (ICD), have traditionally classified
mental health problems on the basis of their putatively distinct
symptom profiles. Yet, this classificatory system omits core
commonalities across these conditions. Despite the historical
dominance of the categorical taxonomic scheme, a growing consensus is emerging that the descriptive taxonomic approach to
psychiatric classification may have reached the limits of its clinical and research utility. Alternative conceptualizations may
afford more fine-grained etiologic and phenomenological
descriptions and therefore may guide clinical practice efforts
more effectively. In that regard, a transdiagnostic perspective
is emerging from cognitive, behavioral, and neuroscientific
research that reveals maladaptive processes underpinning a
broad array of psychosocial maladies commonly addressed by
social work practitioners. Rather than myopically fixating on
distinctions between presumed psychiatric taxons, the transdiagnostic process perspective focuses more broadly on the commonalities bridging the varieties of human suffering. The aim
of the present article is to explicate how a focus on transdiagnostic processes differs from the traditional taxonomic view and
accords more closely with the current evidence from the fields
of experimental psychopathology and neuroscience. To exemplify the transdiagnostic approach, we outline the clinical
features of five key transdiagnostic processes at the root of
human suffering and impaired psychosocial function: automaticity, attentional bias, memory bias, interpretation bias, and
thought suppression. Then, we discuss the implications of the
transdiagnostic approach for social work practice.
On the Origins and Limitations of the DSM
For more than 100 years, various taxonomic systems have
organized the varieties of psychopathological experiences
within distinct diagnostic categories (Kendler, 2009). Influenced by the traditions of the taxonomic biologists and
Linnaean botanists of the 19th century, Emil Kraepelin, the
most prominent of the early psychiatric nosologists, published
his Compendium der Psychiatrie in 1883 (Compton & Guze,
1995). Although Kraepelin was convinced of the biological and
genetic etiology of psychiatric disorders, Compendium der
Psychiatrie was a purely descriptive text, classifying disorders
on the basis of their characteristic patterns of symptomatic
1
College of Social Work, University of Utah, UT, USA
School of Social Work, University of North Carolina at Chapel Hill, NC, USA
2
Corresponding Author:
Eric L. Garland, College of Social Work, University of Utah, Salt Lake City, UT
84112, USA.
Email: [email protected]
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143
expression, prognosis, course, and clinical outcome (Gerard,
2007).
Kraepelin defended his descriptive approach by observing
that
It has been impossible thus far to establish a classification upon an
etiological basis. Although there are some agents that produce very
definite symptoms, such as alcoholic intoxication, certain acute
infectious diseases, head injury, and particularly the more profound forms of hereditary degeneracy, yet very many individual
cases of insanity are wholly without any distinctive etiological features. And furthermore, one often has to admit that any single
pathogenic factor may make itself known by a great variety of
symptoms. Again, the causes of mental disease often work in conjunction with each other, rendering it extremely difficult to ascertain the relationship between the causes and the relationship
between the causes and the symptoms (Kraepelin & Difendorf,
1915, p. 115).
Although the state of psychiatric science at the turn of the
19th century did not allow for the construction of an etiologically informed taxonomy, Kraepelin argued that his approach
had significant advantages over the ‘‘clinical classifications’’
published prior to that time. Criticizing such classifications,
he contended that
The grave defect here arises from the fact that there is apt to be
an overvaluation of some symptoms resulting in the accumulation in one group of all cases having in common some one
striking symptom. In this way, all sad and anxious emotional
states came to be regarded as melancholia, all excited states
as mania, and all delusional states accompanied by hallucinations as paranoia. The difficulty became apparent when a single
case thus classified presents during its course the characteristics
of several groups. It is, therefore, essential . . . to distinguish
between transitory mental states and the disease form itself.
The scientific conception of the disease demands knowledge
not only of the present state, but also of the entire course of the
disease (Kraepelin & Difendorf, 1915, pp. 115-116).
Kraepelin’s focus on the syndromal manifestations and natural histories of psychiatric disorders exerted a prevailing influence on clinical psychiatry and laid the foundation for the
development of the neo-Kraepelinian movement in the United
States, which eventuated in the publication of the third edition
of the DSM in 1980 (American Psychiatric Association [APA],
1980; Palm & Moeller, 2011). Although DSM-I and DSM-II
were brief, poorly formulated, and largely unhelpful guides
to psychiatric diagnosis rooted in psychodynamic formulations
of mental health disorders, DSM-III, with its multiaxial diagnostic system and operationalized criteria sets, is regarded as
perhaps the seminal development in clinical psychiatry over the
last 100 years. Allen Frances, Chairman of the Task Force on
DSM-IV, concluded that ‘‘with these advances DSM-III rescued psychiatry from unreliability and the oblivion of irrelevancy’’ (Frances, 2009, p. 2). In contrast to this claim and in
spite of the significance of DSM-III for psychiatry, empirical
studies reveal that the unreliability of previous editions of the
DSM was not substantially improved with these later revisions
(Kirk & Kutchins, 1994).
Interestingly, although a century had passed since Kraepelin
rejected the possibility of an etiologically based nosology of
psychiatric disorders, Frances (2009) echoed a similar sentiment vis-à-vis DSM-5:
First, let’s expose the absurdity of the DSM-5 claim that it will constitute a ‘‘paradigm shift’’ in psychiatric diagnosis and indicate the
dangers inherent in pursuing this false goal. The simple truth is that
descriptive psychiatric diagnosis does not need and cannot support
a paradigm shift. There can be no dramatic improvements in psychiatric diagnosis until we make a fundamental leap in our understanding of what causes mental disorders. The incredible recent
advances in neuroscience, molecular biology, and brain imaging
that have taught us so much about normal brain functioning are still
not relevant to the clinical practicalities of everyday psychiatric
diagnosis. The clearest evidence supporting this disappointing fact
is that not even one biological test is ready for inclusion in the criteria sets for DSM-5 . . . Descriptive diagnosis is simply not
equipped to carry us much further than it already has. The real
paradigm shift will require an increase in our knowledge—not just
a rearrangement of the furniture of the various descriptive possibilities (Frances, 2009, p. 2).
Although research may not yet provide a solid foundation
for an etiologically informed taxonomy of psychiatric disorders, many practitioners hold out hope for such a taxonomy
in the future. In this vein, McHugh and Slavney (2012) noted
that
The editors of the DSM-5 indicate that the new edition will provide
new categories of disorders, alter some criterion sets, and emphasize matters of severity. But it will not divide psychiatric disorders
into causally intelligible groups. Disregard for this issue—after 30
years’ experience with an appearance-driven policy—makes these
proposed changes for the DSM-5 seem small. The big question—
‘What are these disorders?-will remain unaddressed. . . . Much
turns on causation. For practical psychiatrists, a cause is not some
issue for philosophers to ponder but rather anything that makes a
difference in the evoking or sustaining of a disorder. Causes may
be single or multiple, necessary or sufficient, etiopathic or mechanistic; they are as diverse in human psychological life as the wideranging biopsychosocial model implies. But they must be specified
to render the manifestations of psychiatric illness intelligible and
their treatments rational. (p. 1854)
Beyond its failure to address matters of etiology, other concerns have been raised regarding the DSM nosology. Among
the earliest of these criticisms were those concerning the low
interrater reliability and dubious validity of some disorders
included in the DSM (Andersson & Ghaderi, 2006; Kirk &
Kutchins, 1994). Other observers have stressed that, in several
cases, political factors have seemed to be more influential than
scientific or clinical considerations in determining which disorders were included or excluded from the classification (Kirk &
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Research on Social Work Practice 24(1)
Kutchins, 1992). For example, the public demonstrations of
gay activists outside the halls of the 1974 APA convention
were regarded by many observers as a key determinant of the
organization’s vote that year to declassify homosexuality as a
psychiatric disorder. Likewise, vigorous lobbying efforts by
Vietnam veterans and their supporters were believed to have
influenced the APA’s decision to include posttraumatic stress
disorder (PTSD) in the DSM (Zur & Nordmarken, 2010).
DSM also evidences a number of limitations typical of such
descriptive ‘‘field guides.’’ It often proves difficult, for example, to distinguish conditions that manifest with similar symptoms. To wit: the current controversy regarding appropriate
distinctions between grief, complicated grief, and major
depressive disorder in DSM-5 remains unresolved. (Friedman,
2012). Use of polythetic criteria (i.e., when not all criteria need
to be present to make a diagnosis) and arbitrary diagnostic
thresholds have also been faulted, respectively, for contributing
to excessive heterogeneity within diagnostic categories and to
the current ‘‘epidemics’’ of attention-deficit hyperactivity disorder, childhood bipolar disorder, and autism spectrum disorders (Cooper, Balsis, & Zimmerman, 2010). In addition,
although a maximally useful psychiatric taxonomy for practitioners and researchers alike would include only well-defined
and mutually exclusive sets of disorders and constituent diagnostic criteria, many of the disorder taxons in DSM are overlapping with respect to diagnostic features and related clinical
criteria. For example, impaired attentional and executive function is characteristic of major depression, schizophrenia,
attention-deficit hyperactivity disorder, delirium, and various
substance-related intoxication and withdrawal syndromes.
Diagnostic overlap is also evidenced by the conspicuously high
rates of psychiatric comorbidity observed in population studies
(Kessler, Chiu, Demler, & Walters, 2005). Such comorbidity
may be cross-sectional or longitudinal in nature. In the latter
case, it is common for one disorder to emerge from the development of another disorder (e.g., onset of alcohol dependence
following onset of generalized anxiety disorder, suggestive of
an etiological link).
Other criticisms have been raised in relation to the DSM.
Some observers have decried the burgeoning list of disorders
(now in the hundreds) as yet another indication of the growing
‘‘medicalization’’ and stigmatization of human problems. Others have noted the excessive influence of pharmaceutical companies with regard to disorders selected for inclusion in the
nosology. Still others have accused the APA of profiteering,
given the monumental proceeds the organization takes in from
sales of the DSM and related materials (Kirk & Kutchins, 1992)
or for using psychiatric diagnosis as a means to exercise power
(Greenberg, 2012). Many psychologists have called for functional analyses of maladaptive behavior and individually tailored treatments of mental health disorders, suggesting that
DSM supports a more symptomatically oriented and prescriptive assessment and treatment approach (Andersson & Ghaderi,
2006).
To date, the DSM has evolved through seven editions.
Although each edition has been lengthier and more inclusive
vis-à-vis the number of psychiatric disorders described therein,
the increasing complexity of this descriptive taxonomic
approach to psychiatric classification has not enhanced its clinical and research utility.
A Shift From Traditional Views of Psychopathology to
Transdiagnostic Processes
Over the past decade, an alternative conceptualization of mental health problems has emerged. Instead of categorizing putative psychiatric taxons by their distinguishing features, the
transdiagnostic perspective attends to the common processes
underlying the full panoply of psychological distress and manifold forms of suffering. This view is derived from a mature
body of empirical research that has identified a common set
of cognitive, affective, and psychophysiological processes
across a wide array of diagnoses and conditions. Through the
use of performance-based behavioral tasks, neuroimaging technologies, assessments of autonomic psychophysiology, and
neuroendocrine measures, the biobehavioral correlates of transdiagnostic processes have been delineated and mapped onto
phenomenological reports of persons experiencing psychological distress. In response to the dubious reliability and validity
of the DSM, the National Institute on Mental Health has
advanced a transdiagnostic system for research, the Research
Domain Criteria (RDoC) that integrates information on a wide
array of transdiagnostic processes into a matrix (see http://
www.nimh.nih.gov/research-priorities/rdoc/nimh-researchdomain-criteria-rdoc.shtml#toc_matrix) describing each process
at multiple units of analysis, including genes, molecules, cells,
circuits, physiology, behavior, and self-reports (Insel et al.,
2010). Other transdiagnostic systems have been developed from
the standpoint of clinical practice (e.g., Mansell, Harvey,
Watkins, & Shafran, 2008).
The transdiagnostic perspective acknowledges that psychological states and traits, pathological or otherwise, exist
on continua that may be normally distributed throughout the
general population (Cannon & Keller, 2006; Insel et al.,
2010). For instance, when individuals who do not meet criteria for a major depressive episode diagnosis are experiencing a sad mood state, they are likely to exhibit a negative
memory bias (i.e., they recall more negative than positive
pieces of information; Chepenik, Cornew, & Farah, 2007).
Individuals diagnosed with major depressive disorder exhibit
a more intense yet not qualitatively distinct form of negative
memory bias which intensifies and prolongs their depressed
mood (Mathews & MacLeod, 2005).
The transdiagnostic perspective emphasizes identification
of the homeostatic functions of psychological symptoms over
the apparent structural differences between types of psychological problems. From this point of view, the expression of a
given symptom represents an attempt to adapt to a challenging
environmental context. Lastly, this perspective suggests that
clinical assessment and intervention should directly identify
and target key transdiagnostic processes, rather than gathering
information on diagnosis or allocating different services on the
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basis of separate disorders. In this way, a transdiagnostic
approach to social work practice may be more efficient, parsimonious, and pragmatic, as practitioners can learn how to
assess and intervene with a more circumscribed set of problems
than the plethora of psychopathologies outlined in the DSM.
Next, we discuss five key transdiagnostic processes that underlie a wide range of social, emotional, and behavioral problems
encountered in many direct practice settings.
Automaticity. Although folk psychological notions often propose
that all human behavior is under conscious control, a wide
range of everyday actions and reactions are executed automatically without conscious intention (Bargh & Chartrand, 1999).
Habitual behavior becomes automatized through hundreds of
repetitions of consistent responses to a given stimulus, which
result in rapid stimulus-response (S-R) processing by neural
circuits involved in response execution (Schneider & Chein,
2003). Such automaticity depends upon consistent training of
associations without variation in established S-R relationships
(Shiffrin & Schneider, 1977). During habit formation, behaviors that were initially governed by explicit (i.e., conscious)
associative networks in the brain involving regions of prefrontal cortex and the hippocampus come to be controlled by implicit (i.e., unconscious) sensorimotor corticostriatal circuits
(Wood & Neal, 2007; Yin & Knowlton, 2006). Through this
neurobiological shift, learned behaviors become reflexive
sequences of action that can be evoked without volition or
awareness by conditioned socioenvironmental cues. Furthermore, stress promotes automaticity and inhibits conscious decision making by modulating functional connectivity between
prefrontal cortex and the striatum (Dias-Ferreira et al., 2009).
Although automaticity is an integral component of normal
human learning that enhances efficiency, it may also subserve
patterns of maladaptive cognition and behavior. For instance,
persons with anxiety disorders report experiencing distressing
thoughts that arise in an automatic and unbidden fashion even
when they are identified as irrational and despite efforts to dispel them (McNally, 1995). In a similar vein, people diagnosed
with depression tend to automatically hold negative selfevaluations and predict negative situational outcomes without
conscious effort or intent (Andersen & Limpert, 2001). Automaticity of appetitive behavioral routines is evident in anecdotal reports of alcoholics who describe having the intent to have
only one drink and ‘‘the next thing I knew, the bottle was
empty,’’ previously abstinent crack addicts who describe being
‘‘lost’’ for days in a crack house after relapsing by taking a single ‘‘hit,’’ or the common occurrence of mindlessly bingeing on
snack foods while watching television without awareness of
sensations of satiety or the portion size consumed. Automaticity in addiction is also manifest in studies demonstrating that
addictive behavior is rendered undeterred or insensitive to conditioned aversion (Dickinson, Wood, & Smith, 2002), conditioned cues associated with past drug use episodes can be
processed without awareness (Yan, Jiang, Wang, Deng, He,
& Weng, 2009), more severe substance use is associated with
greater automatization of conditioned responses to substance-
related stimuli (Gladwin & Wiers, 2012), and implicitly processed substance cues reliably predict substance use (Garland,
Franken, & Howard, 2012; Rooke, Hine, & Thorsteinsson, 2008).
Maladaptive forms of automaticity may subvert conscious intention and promote self-destructive behaviors (such as compulsive
substance use, ‘‘cutting’’, or trichotillomania) outside of volition
and awareness.
Attentional Bias. Attention (whether deployed consciously or elicited unconsciously) allows information about motivationally
salient objects or events to gain preeminence in the competition
for information processing resources in the brain (Desimone &
Duncan, 1995). In that regard, attended stimuli receive preferential information processing and thereby are more likely to govern
behavior than unattended stimuli (Corbetta & Shuman, 2002).
Attention gates perceptions of the stimulus to allow for evaluation
of its motivational salience, which in turn facilitates execution of
approach behaviors in response to appetitive objects or avoidance
behaviors in response to aversive ones. Depending on their significance to the self, attended objects elicit approach or avoidance
motivations, while the resultant emotional state further tunes and
directs attention (Friedman & Förster, 2010; Lang & Bradley,
2011). Thus, attention and emotion are tightly coupled in a feedback loop that drives motivated behavior.
People exhibit an attentional bias toward emotionally significant stimuli, evidenced by the automatic capture and fixation
of attention by objects and events that are congruent with their
current mood state (Mathews & MacLeod, 2005). Thus, the
attention of individuals experiencing dysphoric mood is biased
away from neutral or positive stimuli and toward negative objects,
persons, and events. This bias is associated with increased activity
in regions of the brain that process emotional information, such as
the amygdala and anterior insula (Costafreda, Brammer, David,
& Fu, 2008; Frewen, Dozois, Joanisse, & Neufeld, 2008). In the
laboratory, attentional bias can be observed with a dot probe task
when participants exhibit faster reaction times to target probes
replacing emotionally salient images compared with target
probes replacing emotionally neutral images (Field & Cox,
2008). Disorder-specific forms of attentional bias have been
identified among persons diagnosed with anxiety (Cisler &
Koster, 2011), depression (Gotlib, Krasnoperova, Yue, & Joormann, 2004), eating disorders (Brooks, Prince, Stahl, Campbell, & Treasure, 2011), chronic pain (Schoth & Liossi,
2010), substance use disorders (Field & Cox, 2008), and prescription drug use disorders (Garland, Froeliger, Passik, &
Howard, 2012), among others. For example, anxious persons
involuntarily and rapidly orient their attention to threatening
stimuli, which they may then consciously attempt to avoid
(Cisler & Koster, 2011; MacLeod, Mathews, & Tata, 1986).
Despite their deliberate attempts to avoid threatening objects
and events, anxious individuals experience delayed disengagement of attention from threat (Fox, Russo, & Dutton, 2002).
Similarly, individuals diagnosed with substance use disorders
exhibit an automatic orienting of attention toward and delayed
disengagement from substance-related cues like a bottle of
beer or a crack pipe (Field & Cox, 2008). Such addiction
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Research on Social Work Practice 24(1)
attentional bias is associated with craving (Field, Munafo, &
Franken, 2009), exacerbated by stress (Field & Quigley,
2009) and may increase substance use (Field & Eastwood,
2005). Thus, attentional biases cause preoccupation with emotionally significant objects or events, engendering an obsessive
focus that may amplify and perpetuate fear, dysphoric moods,
and addictive behaviors.
Memory Bias. All individuals, whether or not they are struggling
with mental health problems, tend to exhibit mood-congruent
memory, that is, we tend to recall information that is congruent
with our current emotional state (Mayer, McCormick, &
Strong, 1995). Memory tends to be biased toward information
that conforms to the past learning history and current mental
set of the individual. Memory bias may be an evolutionarily
conserved adaptation, in that it may help alert individuals
to potentially dangerous environmental contexts (Schacter,
1999). The presence of objects and events associated with past
occurrences of threat or harm can rapidly and unconsciously
elicit remembered responses; this process of fear conditioning
is mediated in part by the amygdala (LeDoux, 2002). Moreover, by virtue of its functional and anatomic connections with
the hippocampus (involved in processing conscious or ‘‘explicit’’ memories) and the striatum (involved in habit learning;
LaBar & Cabeza, 2006), the amygdala subserves recall of
emotional memories (Richardson, Strange, & Dolan, 2004).
Memories of frightening events may be particularly accessible
to recall, given that such events elicit heightened secretion of
cortisol, a stress hormone that facilitates encoding of threatrelated information into long-term memory by sensitizing
neurons in the amygdala (Rodrigues, LeDoux, & Sapolsky,
2009). However, when sustained over time, elevated cortisol
levels can result in excitotoxic neuron death (McEwen,
2003), which may partially account for altered hippocampal
and amygdala volume among individuals with negative memory bias (Gerritsen et al., 2012).
Negative forms of memory bias have been observed among
individuals meeting DSM criteria for mood and anxiety disorders, who remember a greater proportion of negative than
neutral or positive memories (Mathews & MacLeod, 1994).
Such memory biases are not artifacts of selective reporting
and are evident on tests of implicit (i.e., unconscious) memory
and semantic priming (Watkins, Vache, Verney, Muller, &
Mathews, 1996). For example, when individuals are mired in
a depressed mood, they are more likely to remember losses and
regrets rather than former achievements. Similarly, persons
diagnosed with major depressive disorder report greater frequency of overly general memories than specific memories
(Williams, Teasdale, Segal, & Soulsby, 2000); in other words,
they tend to recall generic synopses of past events rather than
specific incidents. Such biased and overgeneralized forms of
memory may preserve or exacerbate negative mood states by
fueling a cycle of maladaptive cognitive processes, in which
attentional biases form memory biases, which then foster
negative interpretations of current life events based on the negative memories recalled (Garland et al., 2010). Negative
interpretation of present events may bias attention to search for
and encode future negative events, which are then more likely
to be recalled than positive events, resulting in biased and partial accounts of past experience that emphasize narratives of
misfortune and harm.
Interpretation Bias. Many situations and social encounters in
everyday life involve ambiguity. As such, living demands
adaptation to ambiguous contexts, where the outcomes of one’s
actions are uncertain. Adapting to uncertainty induces stress
(Monat, Averill, & Lazarus, 1972) and a sense of loss of control
(Folkman, 1984). To reduce cognitive dissonance generated by
ambiguity, individuals attempt to appraise the meaning of their
experiences according to their life history and integrate this
meaning into their ongoing autobiographical narratives.
Because appraisal of ambiguous situations is conditioned on
past experience, individuals may develop stereotypic ways of
interpreting uncertain events. Thus, individuals may come to
exhibit negative interpretation bias—a tendency to interpret
ambiguous situations and events as having undesirable implications for the self (Holmes, Lang, & Shah, 2009).
Such negative interpretation bias may be evident when clients construe neutral comments as harshly critical and may
be inferred when clients react to events and social encounters
in a consistently negative manner. Moreover, interpretation
bias may be detected with objective, performance-based measures such as the homophone task, in which individuals are
required to spell an audibly presented word that has two possible spellings (one of which is neutral and one of which is emotional; e.g., tents-tense or pane-pain; Pincus & Morley, 2001);
individuals diagnosed with anxiety and major depressive disorders tend to resolve these homophones negatively (Hayes &
Hirsch, 2007; Mogg, Bradbury, & Bradley, 2006) and exhibit
interpretation bias by interpreting ambiguous information
negatively (Mathews & MacLeod, 2005). For instance, when
a person who is experiencing anxiety or a dysphoric mood
attempts to tell a joke in the middle of delivering a public talk
or lecture, and a few individuals respond with laughter, they are
more likely to interpret the people as people ‘‘laughing at
them’’ than ‘‘laughing with them.’’ Individuals in anxious
mood states tend to perceive neutral facial expressions as hostile or upset; such interpretation biases are associated with
hyperactivity in the amygdala coupled with hypoactivity in the
lateral prefrontal and anterior cingulate cortices, a pattern indicative of dysregulated emotional reactivity (Bishop, 2007).
Interpretation bias may maintain psychological dysfunction
by fueling maladaptive, self-confirmatory beliefs with misconstrued evidence that is then taken as veridical truth.
Thought Suppression. In response to unwanted mental experiences, people often attempt to suppress their thoughts and feelings as a means of coping; yet, the effort to not think about
something can paradoxically increase its accessibility to consciousness. In that regard, thought suppression biases attention
toward unwanted cognitions and affective reactions, resulting
in the so-called rebound effects evident in studies in which
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attempted suppression results in enhanced accessibility of the
very thoughts and emotions it is directed against (Wegner,
Schneider, Carter, & White, 1987; Wenzlaff & Wegner,
2000). These rebound effects may be explained by Wegner’s
(1994) ironic process theory, which states that suppression
involves two processes (a) a conscious search for mental contents consistent with the desired psychological state and (b)
an unconscious monitoring process that searches for mental
contents that are inconsistent with the desired state. When the
unconscious monitoring process deploys attention automatically to search for undesirable mental contents to be
replaced, this search results in hyperaccessibility of unwanted
cognitions (Wegner & Erber, 1992). Consequently, the recurrent and intrusive nature of the psychological targets of suppression is amplified by the very process employed to avoid
them (Abramowitz, Tolin, & Street, 2001). Despite the fact that
suppression is intended to decrease emotional responses, it
increases sympathetic nervous system activity, resulting in
heightened physiological stress reactivity evidenced by heightened galvanic skin response, finger pulse amplitude, and pulse
transmission time (Gross & Levenson, 1993). Moreover, the
self-regulatory effort required for thought suppression may
be reflected in increased activation of the anterior cingulate
and dorsolateral prefrontal cortices, brain regions involved
in self-monitoring, and executive function (Mitchell et al.,
2007); such increases in prefrontal cortex activity are coupled
with decreased activation of the hippocampus and amygdala
(Anderson et al., 2004; Depue, Curran, & Banich, 2007).
Because suppression is so cognitively demanding, it depletes
resources required for self-regulation; for instance, among
alcohol-dependent individuals in treatment who attempt to suppress drinking-related thoughts under conditions of stress,
suppression-related neurocognitive depletion is indexed by
attenuated heart rate variability responses to stress and alcohol
cues (Garland, Carter, Ropes, & Howard, 2012).
Suppression is common to many forms of psychological suffering and addictive urges. For example, when asked to suppress
drinking urges following alcohol cue exposure, alcoholdependent individuals evidenced speeded responses to alcoholrelated statements relative to control phrases (Palfai, Monti,
Colby, & Rohsenow, 1997). Such rebound effects have also been
observed for appetitive behavioral habits. Experimental studies in
which participants are induced to suppress thoughts of smoking
(Erskine, Georgiou, & Kvavilashvili, 2010) and eating (Erskine
& Georgiou, 2010) demonstrate that suppression leads to greater
enactment of appetitive behavior. Suppression may also promote
intrusive trauma-related thoughts that are integral to PTSD (Tull,
Gratz, Salters, & Roemer, 2004) by disrupting emotional processing of traumatic memories and obstructing their integration into
long-term memory (Elzinga & Bremner, 2002; Foa & Kozak,
1986). Presumably through such mechanisms, thought suppression significantly predicts the occurrence of PTSD as long as 3
years after a motor vehicle accident (Ehlers, Mayou, & Bryant,
1998; Mayou, Ehlers, & Bryant, 2002). In laboratory research,
experimental induction of suppression of cognitions related to a
traumatic incident resulted in a momentary reduction in thoughts
about the trauma, followed by a resurgence of twice as many
thoughts about the traumatic incident compared to the presuppression level (Beck, Gudmundsdottir, Palyo, Miller, & Grant,
2006). Suppression may also underlie the comorbidity between
conditions; for example, research indicates that among persons
diagnosed with comorbid substance dependence, psychiatric disorders, and extensive trauma histories, thought suppression promotes posttraumatic stress symptoms and drug craving
(Garland & Roberts-Lewis, 2012). When sustained over time,
suppression may exhaust resources for self-regulation, a limited
capacity that is depleted through repeated acts of self-control
(Baumeister, 2003; Muraven & Baumeister, 2000), resulting in
impulsive, unintended, and counterproductive actions.
Discussion and Applications to Social Work
A clinical approach that attends to the aforementioned transdiagnostic processes confers advantages over the DSM/ICD system with regard to the case conceptualization and treatment
planning process that is so essential to direct practice social work
settings. The development of actionable treatment plans
requires clear conceptualization of the pathogenic factors underpinning the presenting problem. Although the diagnosis of
‘‘major depressive disorder’’ suggests the presence of a number
of relatively broad symptom clusters, it may not provide a clinician with the precision needed to guide the selection of effective
interventions for a specific client. In contrast, if the clinician
knows that this specific client fixates his or her attention on indicators of negative social feedback (i.e., an instance of attentional
bias), exclusively remembers past failures (i.e., an instance of
memory bias), interprets ambiguous situations as heralding
disaster (i.e., an instance of interpretation bias), attempts to
ignore unwanted thoughts (i.e., an instance of thought suppression), and compulsively binges on food when stressed (i.e., an
instance of automaticity), identification of such transdiagnostic
processes may help the clinician select a suite of targeted
interventions.
For instance, the clinician could target attentional bias and
automaticity through mindfulness training (De Raedt et al.,
2011; Garland, Gaylord, Boettiger, & Howard, 2010; Garland
& Howard, 2013), memory bias through a historical test of
schema (Padesky, 1994), interpretation bias through cognitive
restructuring (Beck, Rush, Shaw, & Emery, 1979), and thought
suppression through cognitive defusion and acceptance techniques (Hayes, Luoma, Bond, Masuda, & Lillis, 2006). Thus,
case conceptualization through a transdiagnostic approach
points the way directly toward interventive strategies that are
likely to positively influence these processes.
In essence, each transdiagnostic process can be targeted by a
set of interventive techniques grounded in various theoretical
orientations to social work practice. These techniques may
include but are not limited to those which promote (a) exposure
to distressing emotions, cognitions, body sensations, or conditioned socioenvironmental cues (Thyer, 1983); (b) mindful
awareness and regulation of automatic affective and behavioral
reactions (Garland, in press; Hölzel et al., 2011); (c) flexible
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Research on Social Work Practice 24(1)
cognitive reappraisal of stressful life circumstances
as opportunities for learning, meaning, or growth (Garland,
Gaylord, & Fredrickson, 2011); and (d) intentional cultivation
of positive emotions and prosocial actions to foster interpersonal resources and a sense of connection (e.g., Garland, Fredrickson, et al., 2010). Although such techniques can be
delivered from within standard, empirically supported therapeutic approaches (e.g., CBT), novel transdiagnostic intervention packages have been developed and tested (Garland, 2013;
Mansell et al., 2008).
Conclusion
The taxonomies proffered in the current and past versions of
DSM and ICD imply that clinical syndromes can be neatly delineated into orthogonal categories underpinned by distinct biological substrates. In contrast, empirical research over the past
30 years conducted in disciplines ranging from experimental
psychopathology to the neurosciences suggest that a common
set of cognitive, affective, behavioral, and neurophysiological
processes underlie a wide range of psychosocial morbidities.
Many of these processes are prevalent among persons with and
without clinical symptomatology and may have evolved as
conserved adaptations to the demands of survival in a harsh
and dangerous world. Yet, in the context of modern society
where such mortal threats are less commonplace, such processes have become maladaptive and undermine well-being.
Recent findings from cognitive, affective, and neurobiological science indicate that the information-processing capacities
of the human brain can be subverted by automatic habitual
reactions, biased toward negative objects and events, and
depleted through suppression.
Compared with categorical taxonomies, the transdiagnostic
approach is more consistent with a dimensional model of psychological distress and more clearly identifies the processes
whereby unwanted and maladaptive symptoms are produced.
This approach parallels new insights into medicine. Among
oncologists, there is recognition that cancer is extremely heterogeneous, and thus broad diagnostic categories cannot fully
describe the multifarious pathways and mediators that undergird
the disease (Chan & Ginsburg, 2011; Roukos, 2011). Thus,
efforts in ‘‘personalized medicine’’ have been aimed at identifying the specific genetic and environmental mechanisms at play
in a given instance of cancer (Gonzalez-Angulo, Hennessy, &
Mills, 2010; Hamburg & Collins, 2010). This novel approach
is founded on the notion that effective intervention is made possible through the identification of causal agents. At the same
time, cancer involves a number cross-cutting processes (e.g.,
inflammation, metabolic dysregulation, oxidative stress) that
underlie a broad spectrum of physical symptoms found in other
diseases, like heart disease (Andreotti, Porto, Crea, & Maseri,
2002) and diabetes (Haffner, 2006). Unlike cancer, the various
forms of psychological distress and their underlying transdiagnostic mechanisms detailed in this article cannot be reduced to
a mere biological mechanism. Yet, like personalized medicine
in cancer care, a transdiagnostic approach that accounts for
variability stemming from individual differences and factors
common to a wide range of psychosocial problems may hold
considerable utility for social workers engaged in the alleviation
of suffering.
The present discussion is limited in several respects. First,
most of the literature pertaining to transdiagnostic processes
is comprised of studies that compare differences in the magnitude, valence, and content of a given phenomenon (e.g., attentional bias) between individuals who do and do not meet the
criteria for a given DSM diagnosis. To transcend the current
nosology, research on transdiagnostic processes should examine the full range of their expression across the general population using analytic techniques that are sensitive to individual
differences. Second, the majority of studies on transdiagnostic
processes rely on a biobehavioral approach to understanding
the phenomena in question. This is unsurprising, as nearly all
such studies originate from the fields of psychology and neuroscience. Social work, with its unique emphasis and ethical
commitment, would be well positioned to conduct a more holistic form of transdiagnostic research and practice that integrates biobehavioral knowledge with sociocultural, economic,
and political perspectives in understanding and addressing
human suffering.
The processes described in this article do not represent the
sum total of transdiagnostic mechanisms, nor are they exclusively represented by the spectrum of diagnosable conditions
listed herein. To wit, although these processes take various configurations according to the current concerns, emotional state,
and learning history of the individual, there may be common
biopsychosocial structures underlying the diverse clinical presentations of individuals served by social workers. Thus, to be
of greatest benefit to vulnerable persons, we must advance the
field of clinical social work by integrating findings from 21st
century science into models of social work practice that eschew
a single-minded fixation on taxonomy for the more broadminded goal of addressing malleable mechanisms common to
the varieties of human suffering.
Declaration of Conflicting Interests
The authors declared no potential conflicts of interest with respect to
the research, authorship, and/or publication of this article.
Funding
The authors disclosed receipt of the following financial support for the
research, authorship, and/or publication of this article: E.L.G. was
supported in preparing this manuscript by grant R03DA032517 from
the National Institute of Drug Abuse.
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