The British Journal of Psychiatry (2006) 189: 481-483. doi: 10.1192/bjp.bp.106.03825
© 2006 The Royal College of Psychiatrists
Distress and fear disorders: an alternative empirically based taxonomy of the mood and anxiety disorders
Lee Anna Clark, PhD and
David Watson, PhD
Department of Psychology, University of Iowa, Iowa City, USA
Correspondence:
Lee Anna Clark, EIISSH, Department of Psychology, University of Iowa, Iowa
City, IA 52242-1407, USA. Email:
la-clark{at}uiowa.edu
Declaration of interest None.
See pp.
540–546, this
issue. 

ABSTRACT
The nosological organisation of DSM–IV and ICD–10
does not
capture the empirical structure of the mood and anxiety
disorders. Instead,
they form a broad group of internalising
disorders with two
subclasses: distress disorders and fear
disorders. This empirical structure
should form the basis for
revised taxonomies in DSM–V and
ICD–11.

INTRODUCTION
As workgroups begin the task of revising the taxonomy of mental
disorders
and diagnostic criteria for DSM–V and ICD–11,
the field has the
opportunity to bring these classification
schemes in line with current
empirical research. Even if the
DSM–V Task Force adopts a conservative
approach, revising
only those elements for which there is strong empirical
support,
certain sections stand to be radically revised. Only if
non-scientific
considerations play an important part in the revision–or
lack thereof–will these sections see minor rather than
major changes. We
address here two such sections of DSM–IV:
mood disorders and anxiety
disorders.

DEVELOPMENT OF THE CURRENT TAXONOMY
With the advent of DSM–III, a strong separation was made
between
affective and anxiety disorders,
with hierarchical
exclusion rules virtually dictating that
the former trump the latter in cases
in which both types of
disorder were present. Research ignoring these rules
found
no empirical basis for them, however, so they were eliminated
in
DSM–III–R. Once these exclusion rules were relaxed,
research
reports on diagnostic comorbidity flooded the literature.
Clark & Watson
(
1991) and Barlow and
colleagues (e.g.
Barlow et al,
1996) offered theoretical models to explain these
comorbidity
findings, proposing that anxiety and depressive
disorders were linked through
a shared personality dimension
of negative emotionality (or neuroticism;
N/NE), and distinguished
on the basis of unique factors–anhedonia or low
positive
emotionality in depression and autonomic arousal in anxiety.
During the 1990s, the US National Comorbidity Survey data revealed that
major depressive disorder had very different comorbidity rates with various
anxiety disorders, ranging from an odds ratio of 6 with generalised anxiety
disorder to 4 with panic disorder and 3 for simple and social phobia
(Kessler et al, 1996).
Results of genetic studies paralleled the US survey data in that major
depressive disorder and generalised anxiety disorder were found to share a
single genetic diathesis, which also was linked strongly to the N/NE
personality trait (e.g. Kendler,
1996). In contrast, the genetic overlap of major depressive
disorder and other anxiety disorders was lower
(Kendler et al, 1995)
or even negligible (Pauls et al,
1994). Moreover, a review of the voluminous comorbidity literature
by Mineka et al
(1998) revealed that, although
either type of disorder conveyed an increased risk for later development of
the other, anxiety disorders were significantly more likely to appear first,
and cases of pure depression were more rare than pure anxiety, raising the
possibility that anxiety disorders represented a less severe form of a single
spectrum.
These results led Mineka et al
(1998) to propose an
integrative hierarchical model of anxiety and depression with N/NE as a common
genetic substrate, and various specific factors differentiating individual
disorders. Specifically, anhedonia/low positive emotionality is conceptualised
as the specific factor in depression, whereas autonomic arousal represents the
specific component in panic disorder (not anxiety disorders in general, as in
the original model of Clark & Watson,
1991). Other anxiety disorders such as phobias or
obsessive–compulsive disorder also are presumed to have their own
(currently undetermined) specific factors. Fergusson et al
(2006, this issue), using
structural equation modelling on data from a 25-year longitudinal birth cohort
study, found evidence consistent with this model. Specifically, he
demonstrated that a common factor (internalising, on which we
expand subsequently) explained both symptom comorbidities and continuity over
time for major depressive disorder, generalised anxiety disorder, phobias and
panic disorder; at the same time, however, he found across-time continuity in
disorder-specific components of major depressive disorder and phobias.
Although this model explains many aspects of the data well, the exact nature
of the additional specific factors (e.g. whether they are only phenotypic or
also have a genetic basis) remains unclear.

RECENT ADVANCES IN UNDERSTANDING THE STRUCTURE OF PSYCHOPATHOLOGY
An important related question is how the genetic and structural
findings
for anxiety and depression fit into the broader domain
of psychopathology. The
answer to this question has emerged
over the past decade. During this period,
six large-sample
independent studies (
Lahey
et al, 2004; see
Clark, 2005 for
the five
others) have examined the structure of psychopathology
by studying diagnostic
comorbidity patterns phenotypically
and/or genotypically, each using a set of
common mental disorders
that largely overlapped across studies. The results
have revealed
a remarkably consistent structure: a hierarchical model with
two
broad factors–externalising and internalising. Substance
dependence,
attention-deficit hyperactivity disorder, oppositional
defiant disorder, and
conduct disorder/antisocial personality
disorder define the externalising
factor. The internalising
factor subsumes two highly related subfactors:
distress/
misery–comprising generalised anxiety disorder,
overanxious disorder and depressive disorders – and fear,
which includes simple and social phobias, separation anxiety
disorder and
panic disorder. Slade & Watson
(
2006) additionally
showed
that this structure fitted both DSM–IV and ICD–10
conceptualisations of these disorders, with neurasthenia representing
a
manifestation of distress/misery in the latter. Finally,
it is noteworthy that
this alternative hierarchical scheme
consistently captures the comorbidity
data better than the
DSM model, which separates these syndromes into
mood
and anxiety disorders.
The recognition of this structure has engendered further questions about
the nature of the internalising and externalising dimensions themselves. Based
on an extensive review, Clark
(2005) proposed that both
personality (e.g. N/NE) and psychopathology derive from innate general
temperament dimensions, including negative and positive temperament, which
differentiate through development into the full range of adult personality and
also are the diatheses from which psychopathology develops in response to a
sufficiently stressful environment. In this model, internalising emerges
largely from negative temperament and externalising from temperamental
disinhibition, alone or in combination with negative temperament.

IMPLICATIONS FOR DSM–V/ICD–11
Moreover, this robust structure has two important implications
for
DSM–V and ICD–11. First, the hard separation
between mood
disorders and anxiety disorders introduced in
DSM–III, with particular
diagnoses assigned to each group,
is shown to be a pseudo-hierarchical,
rational folk system.
It now is abundantly clear that these two types of
disorders
are strongly related and should not be artificially separated
into
different diagnostic classes. Moreover, the current distinction
between mood
disturbance (the defining element of the current
mood disorders) and
anxiety/avoidance (the characteristic features
of the current anxiety
disorders) is unsound and does not provide
an optimal arrangement of these
disorders (
Watson, 2005). To
the extent that the DSM and ICD purport to be empirical documents,
the current
folk taxonomy must be abandoned and replaced with
a data-driven,
scientifically supported taxonomy. Second, mental
disorders are hierarchically
arranged: that is, the evidence
establishes that most disorders co-occur and
are empirically
related, but that some disorders are more highly comorbid than
others. The taxonomic structures of official diagnostic manuals
need to
reflect this fact.
What this would mean for DSM–V/ICD–11, for example, is that
instead of grouping generalised anxiety disorder, panic disorder, and so on
together under the heading of anxiety disorders, as they are now
in DSM–IV, generalised anxiety disorder and overanxious disorder would
be grouped with major depressive disorder/dysthymia (in what
Watson, 2005, labels the
distress disorders) because they share more variance with these
depressive disorders than with other anxiety disorders. One clear advantage of
such a hierarchical structure is that it reconciles the long-standing tension
between lumpers (who value broad diagnostic categories) and
splitters (who argue for fine-grained diagnostic specificity) by
encompassing both at different levels of the diagnostic hierarchy. Thus,
depending on the nature of the problem at hand, clinicians and researchers can
choose to focus on a few broad non-specific classes of psychopathology (e.g.
distress disorders, externalising disorders), individual disorders, or some
combination of the two. Note also that a hierarchical model easily can be
extended further to encompass subtypes within current disorders (e.g. subtypes
of specific phobia; see Watson,
2005).
The primary immediate change would be organisational, with more highly
comorbid disorders placed together and those with less overlap falling farther
apart in the hierarchical structure. However, although none of the current
diagnoses necessarily would disappear if the empirically revealed structure
were implemented in DSM–V/ICD–11, it is likely that moving to a
more thoroughly empirically based taxonomy eventually would result in more
radical diagnostic revisions. In particular, data-based considerations
eventually would create pressure to replace currently heterogeneous syndromes
(such as many of the current personality disorders) with more homogeneous
diagnostic groups, or at least ones in which observed heterogeneity reflected
more peripheral variation with little implication for differential treatment.
For example, when relations between various personality and psychosocial
variables and treatment outcome were examined in a sample of patients with
recurrent major depression, it was the common, overlapping variance that
carried the predictive weight (Clark et
al, 2003).
There are likely to be pressures from various constituencies to maintain
the status quo, but their bases will be pragmatic rather than scientific. For
example, directors of anxiety disorders clinics may resist revision for fear
that the loss of generalised anxiety disorder to the distress disorders will
reduce their client base. Pharmaceutical companies may express concerns that
extensive (translation: expensive) clinical trials will need to be conducted
to examine the effectiveness of their current antidepressant
drugs for generalised anxiety disorder. Even further, the fact that the
distress and fear disorders are themselves collapsed together at a higher
level in the hierarchy has implications for the cross-effectiveness of
antidepressant and anti-anxiety drugs. Of course,
practising clinicians have known for years that there is no clear one-to-one
correspondence between the formal DSM diagnoses they give their patients and
the prescriptions they write for them, and the pervasive phenomenon of
comorbidity is well known to those who are on the front lines of
mental-disorder treatments. Thus, these pragmatic concerns should not hinder
the development of an empirically adequate and clinically useful psychiatric
classification scheme.

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Received for publication August 27, 2006.
Revision received September 4, 2006.
Accepted for publication September 7, 2006.
Related articles in BJP:
- Structure of internalising symptoms in early adulthood
- DAVID M. FERGUSSON, L. JOHN HORWOOD, and JOSEPH M. BODEN
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