DEPRESSION AND ANXIETY 25:289–299 (2008)
IS GENERALIZED ANXIETY DISORDER AN ANXIETY
OR MOOD DISORDER? CONSIDERING MULTIPLE
FACTORS AS WE PONDER THE FATE OF GAD
Douglas S. Mennin, Ph.D.,1?Richard G. Heimberg, Ph.D.,2David M. Fresco, Ph.D.,3
and Michael R. Ritter, Ph.D.2
Generalized anxiety disorder (GAD) and major depressive disorder (MDD)
demonstrate a strong relationship to each other at both genotypic and phenotypic
levels, and both demonstrate substantial loadings on a higher-order negative
affectivity factor [see Watson, 2005: J Abnorm Psychol 114:522–536]. On the
basis of these findings, there have been a number of calls to reclassify GAD in
the same category as MDD (the ‘‘distress disorders’’). However, any considera-
tion of the reclassification of GAD should also take into account a number of
other factors not only related to GAD and MDD but also to the overlap of these
disorders with other anxiety and mood disorders. First, GAD has established
reliability and validity in its own right, and specific features (e.g., worry) may
become obscured by attempts at reclassification. Second, examination of the
nature of the overlap of GAD and MDD with each other and with other
disorders suggests a more complex pattern of differences between these conditions
than has been suggested (e.g., MDD has strong relationships with other anxiety
disorders, and GAD may be more strongly related to fear than it may first
appear). Third, although findings suggest that GAD and MDD may have
overlapping heritable characteristics, other evidence suggests that the two
disorders may be distinguished by both environmental factors and temporal
presentations. Finally, although overlap between GAD and MDD is reflected in
their relationships to negative affectivity, temporal relationships between these
disorders may be demonstrated by functional changes in emotional responsivity.
Depression and Anxiety 25:289–299, 2008.
& 2008 Wiley-Liss, Inc.
Key words: generalized anxiety disorder; major depression; comorbidity;
diagnosis; DSM-V; emotion
The past two decades have seen considerable
advances in understanding and treating anxiety and
mood disorders. However, despite the delineation of
specific mechanisms (e.g., interoceptive sensitivity in
panic disorder versus fear of negative evaluation in
social anxiety disorder), high levels of comorbidity are
the norm in clinical [Brown et al., 2001a] and
community samples [Kessler et al., 2005b], which
challenges the utility of these specific demarcations.
Further, when multiple disorders are present, reliable
diagnosis can be difficult. Particularly characteristic of
Published online in Wiley InterScience (www.interscience.wiley.
Received for publication 22 February 2008; Revised 22 February
2008; Accepted 25 February 2008
?Correspondence to: D. S. Mennin, Ph.D., Department of
Psychology, Yale University, P.O. Box 208205, New Haven, CT
06520. E-mail: email@example.com
1Department of Psychology, Yale University, New Haven,
2Department of Psychology, Temple University, Philadelphia,
3Department of Psychology, Kent State University, Kent, Ohio
rrrr 2008 Wiley-Liss, Inc.
this difficulty is generalized anxiety disorder (GAD),
the nosological integrity of which has been criticized
[for a review, see Mennin et al., 2004]. Although the
reliability and validity of GAD have improved con-
siderably because worry was established as its central
feature, GAD exhibits high rates of comorbidity with
unipolar mood disorders [see Brown et al., 2001a;
Kessler et al., 2005b], which may reflect a shared
genetic diathesis [e.g., Kendler et al., 1992].
Watson [2005, 2008] criticized the rationally derived
diagnostic classification system in Diagnostic and
Statistical Manual of Mental Disorders (DSM-IV) [Amer-
ican Psychiatric Association ,1994] for categorizing
disorders on the basis of shared phenomenological
features rather than empirical data. He explained that
this system assumes weak relationships across diag-
nostic categories (e.g., social anxiety disorder and
dysthymia) and stronger relationships within a diag-
nostic category (e.g., social anxiety disorder and
posttraumatic stress disorder) and, thus, cannot directly
account for the high levels of comorbidity that often
occur across diagnostic categories (e.g., between GAD
and major depressive disorder (MDD)). Citing findings
from epidemiological samples, he explained that the
overlap between GAD and MDD is substantial
[tetrachoric correlations between disorders range from
.59 to .70; see Kessler et al., 2005b; overlap between
these disorders is also high in clinical samples; see
Brown et al., 2001a]. Further, he reviewed structural
modeling studies that examined either symptom
patterns or diagnoses [e.g., Brown et al., 1998; Krueger
et al., 1999; Watson et al., 1995], finding a high degree
of association between GAD and MDD, with both
disorders loading most strongly on a higher-order
factor of negative affectivity (i.e., neuroticism, distress).
Watson reviewed genotypic data [e.g., Krueger RF,
1999] suggesting that GAD and MDD are virtually
indistinguishable. Finally, Watson also noted that both
conditions respond to treatment with serotonin and
norepinephrine reuptake inhibitors, further suggesting
a shared relationship between GAD and MDD.
Given this substantial overlap, some investigators
have questioned whether GAD should be diagnosed
independently of MDD in DSM-V. Proposed changes
for DSM-V include (1) placing these disorders with
dysthymia and posttraumatic stress disorder in a
category of ‘‘distress disorders’’ [Watson, 2005], which
would be distinguished from a ‘‘bipolar disorders’’
category (comprising bipolar I, II, and cyclothymia)
and a ‘‘fear disorders’’ category comprising the
remaining DSM-IV anxiety disorders (e.g., panic
disorder, specific phobia, and social anxiety disorder)
with the exception of obsessive compulsive disorder; (2)
recategorizing GAD as a mood disorder [Vollebergh et
al., 2001]; (3) subsuming GAD under MDD as a
subtype similar to ‘‘agitated depression’’ [see Kendler
et al., 1996]; or (4) using a broader category such as
neuroticism to capture both disorders, with the
purpose of increasing predictive power and accounting
for the overlap that is seen in genotypic and phenotypic
investigations [Andrews, 1996]. The architects of
DSM-V and leading mood and anxiety disorders
researchers are currently reviewing these suggestions
as an alternative to the position that GAD should
continue to be classified as an anxiety disorder (for
more information, see ‘‘The Future of Psychiatric
Diagnosis: Refining the Research Agenda (Depression
and Generalized Anxiety Disorder Research Planning
Although GAD and the unipolar mood disorders are
significantly related, removing GAD from the anxiety
disorders may be premature for two main reasons. First,
this decision may not fully reflect the complex relation-
ship that GAD shares with both mood and anxiety
disorders. Second, the decision to remove GAD from
the anxiety disorders arises without fully accounting for
the relationship between mood disorders and anxiety
disorders other than GAD. In the remainder of this
paper, we consider six issues that challenge the
arguments and suggestions of Watson [e.g., 2005,
2008] as well as others who favor separating GAD
from the other anxiety disorders. Specifically, we
explore whether (1) arguments to remove GAD from
the other anxiety disorders are predicated on miscon-
ceptualizations of the diagnostic integrity of GAD,
which has actually established greater reliability and
validity as a diagnostic category than credited; (2) the
degree of comorbidity between MDD and GAD is not
unique to GAD and may also reflect a tautology based
on the symptoms chosen to define the disorders in
DSM-IV; (3) structural findings regarding symptom
clustering may reflect these symptom inclusion deci-
sions and, thus, may be alternatively interpreted to
support retaining GAD as an anxiety disorder through a
delineation of the relationship of MDD with fear
disorders and fear processes within GAD; (4) although
GAD and MDD may share common genetic diatheses,
environmental factors distinguish these disorders and
may account for both similarities and differences in
treatment efficacy; (5) given environmental influence in
the expression of GAD or MDD, the examination of
functional relationships between the disorders may
provide a greater understanding of these disorders than
reliance on structural relationships alone; and (6) rather
than favoring ‘‘lumping’’ or ‘‘splitting,’’ categorization
can reflect both higher- and lower-order relationships,
possible diatheses and stress factors, and the temporal
relationship of these conditions if both structural and
functional associations between the disorders are
considered in nosological decisions regarding the over-
lap between GAD and mood disorders.
INTEGRITY OF THE DIAGNOSIS
Many investigators cite the history of poor reliability
of GAD as evidence for the need to reclassify. Other
290 Mennin et al.
Depression and Anxiety
common criticisms of GAD are that it is not associated
with independent contributions to impairment or
distress and that it lacks clear and specific mechanisms
that could differentiate it from other conditions.
Although early versions of GAD suffered considerably
from low reliability and poor validity, GAD as defined
in the DSM-IV has, to the contrary, achieved
diagnostic reliability on par with other anxiety and
mood disorders and demonstrated unique mechanisms
and patterns of impairment.
Early investigations into the reliability of GAD
provided little support for the diagnosis. Interrater
reliability of GAD based on DSM-III [American
[k5.47; DiNardo et al., 1983]. Reasons for low
reliability may have included the lack of a clear marker
for the condition and the inclusion of many nonspecific
physical symptoms. However, worry became the
essential feature of GAD in the DSM-III-R [American
Psychiatric Association, 1987]. Sanderson and Barlow
 found that the presence of worry could be
reliably detected, with a k coefficient of .90. DSM-IV
further clarified the diagnosis by focusing physical
symptoms around chronic levels of tension and
removing symptoms that more likely to reflect acute
autonomic arousal. This change reduced rates of
comorbidity with other anxiety disorders, increased
the specificity of these physical symptoms [e.g.,
Joormann and Sto ¨ber, 1999; Marten et al., 1993], and
improved interrater reliability of GAD (k5.67 for
current diagnosis), putting it on par with other
disorders such as MDD [k5.67 for current diagnosis;
Brown et al., 2001b].
criteria was poor
Numerous studies demonstrate that GAD (with or
without comorbid MDD) is associated with significant
impairment and distress. Primary-care patients with
noncomorbid GAD reported more disability days (in a
1-month period) and poorer social functioning than
other primary-care patients [e.g., Ormel et al., 1994].
Kessler et al.  examined the National Comor-
bidity Survey and the Midlife Development in the
United States Survey and found that noncomorbid
GAD and noncomorbid MDD had comparable rates of
perceived mental health and social impairment and that
these results were not due to co-occurring psycho-
pathology or demographic variables. Wittchen et al.
 examined individuals assessed as part of the
German National Health Interview and Examination
Survey and found that groups with noncomorbid GAD,
noncomorbid MDD, and co-occurring GAD and
MDD had equivalently high levels of social and work
impairment after controlling for demographic variables
and other forms of psychopathology. Further, indivi-
duals with noncomorbid GAD reported poorer quality
of life than individuals with noncomorbid MDD. Stein
and Heimberg  reanalyzed data from the Ontario
Health Survey Mental Health Supplement to deter-
mine therelative impact
co-occurring GAD and MDD. The effects of GAD
were examined while statistically controlling for the
effects of MDD. Lifetime GAD was independently
associated with an increased likelihood of dissatisfac-
tion with the respondent’s main activity and an
increased likelihood of dissatisfaction with family
life. Both past-year and lifetime GAD were signifi-
cantly associated with an increased likelihood of low
overall perceived well-being. Taken together, these
investigations suggest that both GAD and MDD
demonstrate significant, yet distinguishable, associa-
tions with impairment.
ofeach disorder in
Increases in reliability and delineation of the essential
criteria for a diagnosis of GAD have led to the
delineation of pathological mechanisms with greater
specificity [see Borkovec et al., 2004]. Worry is more
elevated in GAD than other anxiety and mood disorders
[e.g., Chelminski and Zimmerman, 2003]. In addition,
considerable evidence indicates that cognitive biases can
differentiate GAD from MDD [for a review, see Mineka
et al., 2003]. In particular, GAD, but not MDD, has
shown strong associations with attentional biases to
threatening stimuli. In contrast, memory biases are more
common in MDD than GAD. Recently, other con-
structs have demonstrated patterns of specificity with
GAD. Intolerance of uncertainty, which refers to one’s
characteristic difficulty with ambiguous and uncertain
possibilities, has been found to be elevated in individuals
with GAD compared to those with other anxiety and
mood disorders, including MDD [see Dugas et al.,
2004], although intolerance of uncertainty is also
elevated in obsessive compulsive disorder [Holaway et
al., 2006]. In contrast, individuals with MDD, but not
GAD, appear to have a greater certainty that negative
events will occur [e.g., Miranda and Mennin, 2007].
Emotion-related deficits have also differentiated GAD
from MDD [Mennin et al., 2007]. In particular, GAD
was uniquely related to greater emotional reactivity and
dysregulation, when variance associated with MDD was
constrained. In contrast, MDD had a specific relation-
ship with poor ability to understand emotional informa-
tion and negative beliefs about the consequences of
experiencing emotions, when variance associated with
GAD was constrained. Finally, although some biological
mechanisms appear to be nonspecific (e.g., 5-HTsystem
deficiencies), robust findings indicate a role of GABA/
benzodiazepine receptor dysfunction in GAD, but not
MDD [cf., Lydiard and Monnier, 2004].
Structural models of diagnostic overlap have demon-
strated that GAD and MDD load onto a higher-order
291Is GAD an Anxiety or Mood Disorder?
Depression and Anxiety
factor of generalized negative emotional distress
(labeled ‘‘Anxious/Misery’’ or ‘‘Distress’’ in these
studies) using both lifetime [Krueger et.al., 1999]
and 12-month [Vollebergh et al., 2001] diagnoses.
Further, in these studies, this factor was distinguished
from a ‘‘Fear’’ factor on which panic disorder,
disorder loaded. However, a stronger test of the
overlap between GAD and MDD comes from the
examination of symptom sets rather than diagnoses,
given that diagnoses are confounded by the categoriza-
tion system from which they are derived [Brown and
Barlow, 2005]. In studies examining symptom-level
items related to anxiety and mood pathology [e.g.,
Watson et al., 1995], clusters of symptoms map onto
three factors, which correspond to different aspects
of emotionality, including heightened negative emo-
tionality, reduced positive emotionality, and heightened
autonomic arousal. Symptoms reflective of general
anxiety and depressive symptoms both most strongly
mapped onto negative emotionality, as in the diagnostic
structural models, but only depressive symptoms
mapped onto positive emotionality and only anxious
symptoms mapped onto the autonomic arousal factor.
One drawback to these symptom-level studies was
the reliance on nonclinical samples. In contrast, Brown
et al. , examining both self-report symptom
levels and diagnoses in a large patient sample,
replicated findings that GAD and MDD factors
(comprising both self-report and diagnostic data)
shared an association with negative emotionality.
Further, MDD and social anxiety disorder, but not
GAD, were associated with low positive emotionality.
In addition, GAD, but not MDD, was negatively
related to autonomic arousal suggesting autonomic
suppression [consistent with experimental findings in
GAD; see Borkovec et al., 2004].
These findings not only support the relationship
between GAD and MDD but also demonstrate
important areas of divergence that should give us
pause before making classification decisions based on
structural overlap. First, the specificity of the relation-
ship between GAD and MDD appears to be affected by
the nature of inputs to the structural models, which
reflect a tautology given the considerable symptomatic
overlap in the DSM-IV criteria for these disorders.
In addition, the findings from Brown et al. 
concerning the convergence of MDD and social
anxiety disorder in relation to low positive affectivity
as well as other sources reviewed below suggest a
and anxiety disorders other than GAD. Finally,
the relationship of autonomic suppression to GAD,
but not MDD, in the Brown et al.  study, as well
as other findings reviewed below concerning the role of
fear in GAD, suggest that fear processes may be
important in GAD but obscured by compensatory
mechanisms such as worry. These points are expanded
SYMPTOMATIC OVERLAP BETWEEN GAD
AND MOOD DISORDERS
Although the diagnostic structural analyses [Krueger
et al., 1999; Vollebergh et al., 2001] reflecting
the loadings of GAD and MDD on a higher-order
factor were most robust, symptom-based structural
models have been equivocal, with some showing
superiority when GAD and MDD are combined
in latent factors [e.g., Watson et al., 1995] and another
showing superior fit when these disorders are kept
separate [Brown et al., 1998]. One explanation for
these heterogeneous results is the nature of the
inputs submitted for modeling. Models limited to
DSM-IV diagnoses or symptom clusters were most
likely to find structural harmony for GAD and MDD.
However, such inputs to the model are highly related
by design (i.e., overlap between GAD and MDD may
be partially a product of poor measurement of the
distinction between the conditions). In contrast, Brown
et al.  utilized DSM-IV diagnoses and symptoms
as well as additional measures of closely related
processes such as worry [Penn State Worry Ques-
tionnaire; Meyer et al., 1990] and social interaction
anxiety [Social Interaction Anxiety Scale; Mattick and
Clarke, 1998]. Similarly, other analyses examining the
overlap between mood and anxiety symptoms have
shown greater distinctiveness in the conditions when
anxious apprehension, assessed with the Penn State
Worry Questionnaire, was included [e.g., Heller and
Although the diagnostic criteria for GAD in the
DSM-IV reduced rates of comorbidity with other
anxiety disorders and increased the specificity of its
physical symptoms [e.g., Marten et al., 1993], they
Undoubtedly, the entities of ‘‘GAD’’ and ‘‘MDD’’ are
both related to negative affectivity. Indeed, the emo-
tions of fear/anxiety and sadness, the essential phe-
nomenological ingredients of anxiety and unipolar
mood disorders, have also been shown to map onto
higher-order factors of negative affectivity [see Watson,
2005, 2008]. However, defining GAD and MDD using
highly overlapping symptoms may obscure important
distinctions between these disorders as well. A quick
look at the diagnostic criteria for GAD reveals that four
out of the six associated physical symptoms (i.e.,
restlessness, fatigue, difficulty concentrating, sleep
difficulties) are also part of the diagnostic criteria for
MDD. In addition, four of the symptoms required for
MDD (i.e., sleep difficulties, psychomotor agitation,
fatigue, difficulty concentrating) overlap with GAD.
(i.e., sleep difficulties, fatigue, difficulty concentrating)
also overlap with GAD. Given that three of these
symptoms are required for GAD, five for MDD, and
two for dysthymia, there is a high likelihood that
individuals could meet criteria for GAD or a mood
disorder with symptoms fully reflective of GAD (and
292Mennin et al.
Depression and Anxiety
vice versa). Thus, it remains a question as to whether
individuals who meet criteria for these diagnoses with
overlapping symptoms are best described as having
GAD, MDD, or both.
Brown et al. [2001b], noting the prominent overlap
of GAD and MDD, suggested that GAD could be
further refined to promote better separation from the
mood disorders. Indeed, examinations of the six
retained physical symptoms of GAD have shown
discriminant validity between GAD and the other
anxiety disorders but have not discriminated strongly
between GAD and MDD [e.g., Joormann and Sto ¨ber,
1999; Kubarych et al., 2005]. Joormann and Sto ¨ber
 explored the ability of DSM-IV symptoms of
GAD to discriminate depressive symptomatology from
worry. Although the majority of current symptoms of
GAD were not well differentiated from depression,
muscle tension appeared to be uniquely related to
worry and difficulty concentrating appeared to have
a particularly strong relationship with depression.
Indeed, muscle tension was negatively related to
depression in this study. Kubarych et al.  also
found muscle tension, but not other DSM-IV symp-
toms of GAD, to be unique to the disorder in a factor
analysis of a large sample of female twins. These
findings of the specificity of muscle tension to GAD
are noteworthy given that physiological studies have
also found differences between GAD and healthy
controls [e.g., Hoehn-Saric et al., 1989]. One might
question whether muscle tension was emphasized and
difficulty concentrating de-emphasized, whether the
patterns of co-occurrence between GAD and MDD
might be altered.
Other symptoms, not currently included in the
DSM-IV criteria for GAD and MDD, might help to
further differentiate these disorders. Intolerance of
uncertainty [Dugas et al., 2004] and subjective emo-
tional reactivity [i.e., affect intensity; Mennin et al.,
2007] are two possible candidate symptoms. Prelimin-
ary findings suggest that the inclusion of one item
inquiring about intensity of emotional responses
increases distinctiveness of GAD in relation to MDD.
Another possibility for increasing distinctiveness of
GAD is to alter what might be overly restrictive criteria
in the current symptom set. Ruscio et al.  found
that when worry was not required to be excessive to
meet criteria for GAD, comorbidity with MDD and
dysthymia decreased, although GAD without excessive
worry remained comparable to the original diagnosis in
persistence, impairment, treatment-seeking, and family
aggregation. Further, Kessler et al. [2005a] found a
similar result when the duration of GAD was reduced
from 6 months to 1 or 2 months. One possibility that
has been offered by Kessler et al.  for the high
comorbidity of GAD is its low prevalence in compar-
ison to MDD, which might inflate co-occurrence of
disorders given less variance available for heterogene-
ity. It may be that decreasing arbitrarily restrictive
criteria increases prevalence rates (as both of these
criteria changes did) and, subsequently, decreases
the effect of comorbidity. Interestingly, bipolar II
comorbidity did not decrease as a result of the duration
change in the Kessler et al. [2005a] study. This
argument is consistent with a recent analysis of the
comorbidity rates of bipolar disorders in the National
Comorbidity Survey Replication , which demonstrated
a strong relationship of both bipolar I (39%) and
bipolar II (37%) disorders with GAD, and a study
of comorbidity in a Hungarian epidemiological sample
in which rates of comorbidity with GAD were higher
in bipolar II disorder (21%) than MDD [14%; Rihmer
et al., 2001]. These results suggest that classification
of GAD and the mood disorders should reflect
relationships with bipolar as well as unipolar mood
disorders. Despite these encouraging possibilities for
modifying GAD criteria, its important to also note that
some changes might lead to increases in the overlap
between GAD and MDD, such as lifting the hierarch-
ical requirement between the conditions (i.e., GAD
cannot be diagnosed when MDD is temporally over-
lapping), which has been shown to increase rates of
GAD in individuals with MDD [Zimmerman and
SYMPTOMATIC OVERLAP BETWEEN MDD
AND OTHER ANXIETY DISORDERS
Although GAD and MDD are highly overlapping in
epidemiological [Kessler et al., 2005b] and clinical
[Brown et al., 2001a] samples, these same sources of
data also show strong relationships between the
unipolar mood disorders and the ‘‘fear disorders’’ such
as social anxiety disorder and panic disorder. For
example, MDD was highly related to GAD (tetrachoric
correlation of .62) but also showed strong relationships
to panic disorder (.48), agoraphobia (.52), social anxiety
disorder (.52), and specific phobia (.43) in the National
Comorbidity Survey Replication. With dysthymia, the
correlations with GAD and other anxiety disorders are
almost indistinguishable. Tetrachoric correlations with
dysthymia were equivalent for GAD (.55), social
anxiety disorder (.55), and panic disorder (.54) and
were only slightly lower for specific phobia (.44) and
agoraphobia (.44). Slade and Watson  analyzed
epidemiological data from the Australian National
Survey of Mental Health and Well-Being and found
similar tetrachoric correlations between the mood
disorders and other anxiety disorders (correlations
ranged from .50 to .56). Analysis of data from the
clinical sample of Brown et al. [2001a] produced similar
patterns of overlap between MDD and the other
anxiety disorders. Rates of co-occurrence between
MDD and GAD (57% with hierarchy rules lifted)
were not greatly different than the rates with social
anxiety disorder (43%) or panic disorder with or
without agoraphobia (46%). For dysthymia, the rates
of overlap with GAD were comparable to social anxiety
disorder (56%) but higher than panic disorder with or
293Is GAD an Anxiety or Mood Disorder?
Depression and Anxiety
without agoraphobia (34%). Interestingly, panic dis-
order with agoraphobia (b5.65) loaded on the
negative affectivity higher-order factor to almost the
same degree as MDD (b5.67) in the Brown et al.
[2001b] structural equation modeling study. Similarly,
using the data from the original National Comorbidity
Survey , which utilized DSM-III-R criteria, Weinstock
and Whisman  found that noncomorbid GAD
and noncomorbid panic disorder did not differ
significantly in rates of neuroticism (i.e., negative
affect), but pure MDD had considerably lower rates.
Another consideration in pondering the overlap
of mood disorders with other anxiety disorders versus
GAD is the role of positive affectivity in MDD
and social anxiety disorder. A strong relationship
has been found between MDD and reduced positive
affectivity [e.g., Watson et al., 1995]. Similarly, a
diminished response to positive stimuli in MDD has
also been demonstrated in experimental settings using
subjective, expressive, and psychophysiological indices
[e.g., Rottenberg et al., 2002]. A recent meta-analysis
[Bylsma et al., 2008] of laboratory studies found that,
although individuals with MDD were characterized by
reductions in emotional reactivity to both positively
and negatively valenced stimuli, effects were stronger
for positive stimuli (d5?.53) than for negative stimuli
(d5?.25). However, low positive affectivity does not
appear to be specific to MDD. In the Brown et al.
 structural equation model, GAD did not
demonstrate a relationship with positive affectivity,
but both MDD and social anxiety disorder did (b’s of
?.29 and ?.28, respectively).
Kashdan  provided theoretical and empirical
support for the unique role of low positive affectivity in
social anxiety disorder. In a meta-analysis of 34 studies,
social anxiety was significantly negatively associated
(r5?.24), a trait associated with appetitive motivation.
Further, these associations remained significant after
controlling for depressive symptoms or diagnoses
(r’s5?.21 for both positive affectivity and curiosity).
Kashdan interprets these meta-analytic findings within
a self-regulatory framework. He suggests that excessive
self-evaluative concern may lead to avoidant regulatory
actions in service of anxiety reduction that interfere
with reward and promotion behaviors. Similar to
behavioral perspectives on depression [e.g., Libet and
Lewinsohn, 1973], if an individual withdraws from a
potentially rewarding context due to avoidance, the
likelihood of future rewarding circumstances might
diminish. However, one might expect that the reasons
for withdrawal from rewarding contexts might be
different for social anxiety (i.e., avoidance of perceived
threat) than for depression (i.e., decreased value of
volitional processes of the reward stimulus). None-
theless, it appears that the decreased positive emotions,
not central to GAD, are an important component of
both social anxiety disorder and depression. Consistent
with these findings, Mennin et al.  found that
MDD and social anxiety, accounting for each other’s
variance as well as that of GAD, were both character-
ized by a poor understanding of emotions and negative
beliefs about the consequence of emotions, including
positive affect. Interestingly, when MDD and social
anxiety were controlled, GAD showed no relationship
to these emotion variables, suggesting that social
anxiety and MDD may share a broader pattern of
emotional characteristics involving regulatory re-
sponses to emotions in addition to levels of emotional
experience (i.e., reduced positive affectivity).
SYMPTOMATIC OVERLAP BETWEEN GAD
AND OTHER ANXIETY DISORDERS:
IS THERE FEAR WITHIN GAD?
Removing autonomic symptoms from the criteria for
GAD in DSM-IV increased specificity with the other
anxiety disorders [e.g., Marten et al., 1993] but may
have also led to the obfuscation of the role of
fear processes in generalized anxiety and worry.
Despite the removal of autonomic symptoms, DSM-
IV GAD was highly correlated with ‘‘fear disorders’’
including panic disorder (.46), agoraphobia, (.45), and
social anxiety disorder (.47) in the National Comor-
bidity Survey Replication [Kessler et al., 2005b]. These
correlations were similar to the association found for
social anxiety disorder and panic disorder (.48). In
the Australian National Survey of Mental Health
and Well-Being sample, Slade and Watson 
found similarly high tetrachoric correlations for GAD
and panic disorder (.62), agoraphobia (.61), and social
anxiety disorder (.58), which were not well distin-
guished from the associations between social anxiety
disorder and panic disorder (.59). Consistent with these
reported rates, Maier et al.  examined the role of
the autonomic symptoms that comprise the diagnosis
of GAD in ICD-10 (but were removed from DSM-IV)
and found that there were strong relationships between
these symptoms and persistent worry and anxiety.
These relationships suggest that, at least for a subgroup
of individuals with GAD, fear processes may be an
important component of their anxious presentation.
Indeed, despite the formal removal of the autonomic
symptoms from the DSM-IV criteria set, limited
symptom panic attacks are often seen clinically in
patients with GAD.
In contrast to the increased autonomic activity
demonstrated by these associations, Brown et al.
 demonstrated that, whereas panic disorder was
positively associated with an autonomic arousal factor,
GAD was negatively associated with this same factor.
Interestingly, MDD and social anxiety disorder were not
significantly related to this factor, providing further
support for a more complex relationship among GAD,
MDD, and social anxiety disorder than previously
thought. But how can we explain positive correlations
between ‘‘fear disorders’’ (e.g., panic disorder) and GAD
in the context of an inverse structural relationship? The
294 Mennin et al.
Depression and Anxiety
answer likely lies in the function of worry in GAD. As
mentioned above, Brown et al.  used multiple self-
report and diagnostic indices to represent GAD,
including the Penn State Worry Questionnaire and
other process measures of worry. This greater focus on
worry may account for the negative relationship with
autonomic arousal. In numerous studies, worry has been
related to autonomic inflexibility in GAD [e.g., see
Borkovec et al., 2004; Hoehn-Saric et al., 1989].
Borkovec and colleagues have developed one of the
most prominent and well-supported models of worry in
GAD. This model asserts that worry serves an avoidant
function by suppressing autonomic hyperarousal. This
functional relationship has been repeatedly demon-
strated, and there would be little to suppress if persons
with GAD did not cycle through periods in which they
were overwhelmed by these symptoms. Most likely,
worry is enacted, in part, as a response to autonomic
activity, to which individuals with GAD have reported to
have more sensitivity than other individuals [i.e., anxiety
sensitivity; see Rector et al., 2006]. Thus, autonomic
activity may be obscured by the engagement of worry.
Further support for this functional relationship between
autonomic activity and worry comes from the estab-
lished clinical finding of ‘‘relaxation-induced anxiety,’’ in
which patients with GAD engaged in relaxation-
encouraging exercises (e.g., progressive muscle relaxa-
tion; diaphragmatic breathing) experience a surge in
autonomic activity, often experienced as a limited
symptom panic attack [see Heide and Borkovec, 1983].
Although speculative, the notion that worry serves as
a compensatory mechanism could also be gleaned from
the developing neurobiological literature. For example
adults with GAD evidence elevated levels of dorsolat-
eral prefrontal cortical activation [Mathew et al., 2004].
This area is typically associated with effective executive
control of negative emotions yet it is showing increases
in symptomatic individuals with GAD—potentially
showing a compensatory mechanism at play. Interest-
ingly, children and adolescents with GAD, who
presumably do not have the same level of cognitive
function, do not display this same level of dorsolateral
prefrontal activation but do display elevated amygdalar
activity [i.e., suggestive of fear processes; DeBellis
et al., 2000; McClure et al., 2007]. It may be that, as
individuals with GAD get older and their cognitive
abilities get stronger, they rely more on worry, as
Borkovec would suggest, to constrain fear responses.
Worry may be reinforced by fear reduction, suggesting
that although it may be obscured, fear still plays an
important motivational role in GAD.
Delineation of temperamental markers reflective
of a higher-order personality factor (i.e., neuroticism,
negative affectivity) that are reliable, predictive of
psychopathology, and associated with identifiable
biological markers [e.g., human serotonin transporter
gene, SLC6A4; see Hariri et al., 2002] have clear value
to our etiological understanding of the anxiety and
mood disorders. However, they are unlikely to fully
account for all phenotypic presentations of these
disorders, even ones most strongly related to higher-
order personality factors such as GAD and MDD.
Despite the robust and similar heritability ratings for
these disorders, numerous environmental and develop-
mental factors distinguish their expression. Further, the
proximal etiologic relationship between GAD and
MDD is likely a temporally functional one with GAD
more likely to precede MDD. Thus, rather than
focusing exclusively on structural relationships between
these disorders, examinations of the functional emo-
tional relationships between GAD and MDD may
elucidate how these disorders converge and diverge.
Meta-analytic investigations of familial and genetic
factors demonstrate that GAD and MDD are asso-
ciated with moderate levels of heritability [37 and 32%,
respectively; Hettema et al., 2001; Sullivan et al., 2000].
Family studies have demonstrated that rates of GAD
are elevated in first-degree relatives of both GAD and
MDD probands [e.g., Kendler et al., 1997]. Further,
Kendler et al.,  have demonstrated strong
heritability relationships between GAD and MDD .
These studies consistently show that genetic factors are
almost entirely shared between these disorders, but
shared environmental variance is quite modest. Mineka
et al.  suggested that this shared genetic factor
likely reflects individual differences in general distress
and negative affectivity. Indeed, studies indicate that
neuroticism is highly genetically related to both GAD
[Hettema et al., 2004] and MDD [Fanous et al., 2002],
with a stronger effect for GAD. However, the genetic
overlap between GAD and MDD is only moderately
related to the genetic overlap of neuroticism with each
disorder [e.g., Hettema et al., 2006], suggesting that,
even at the genetic level, other factors beyond
dispositional emotionality may account for the shared
inheritance of GAD and MDD. Consistent with these
genetic data, measures of emotionality such as neuroti-
cism have been found to predict comorbidity patterns
in these disorders [e.g. Chambers et al., 2004], yet a
significant number of individuals with elevations on
these dispositional variables do not have GAD or
MDD [e.g., Rettew et al., 2006]. Further, Kessler et al.
 warned that these results should be interpreted
with caution, because models in these studies assume
that the joint effects of genes and environment are
additive and, thus, ignore genetic influence on envir-
onment. Likely, the role of genotypic variables in GAD
and MDD are heterogeneous as are their effects on
phenotypic presentations. More research is clearly
needed to delineate how genetic factors in GAD,
MDD, and neuroticism may interact and influence
295Is GAD an Anxiety or Mood Disorder?
Depression and Anxiety
Various stressors (e.g., traumatic events, loss) may
interact with the same diathesis (e.g., heritable factors)
to produce different outcomes. Indeed, although
between GAD and MDD, environmental factors
appear to diverge to a greater degree [e.g., Kendler et
al., 1992]. Few studies have examined patterns of
environmental factors between DSM-IV diagnoses of
GAD and MDD. However, recently, Moffitt et al.
 examined risk factors associated with nonco-
morbid GAD, noncomorbid MDD, and comorbid
MDD and GAD in the 1972–1973 Dunedin birth
cohort of 1,000 individuals followed to age 32 (with
96% retention). Individuals with noncomorbid GAD
demonstrated a discernable pattern of stressors (i.e.,
maltreatment, low SES, childhood behavior problems)
compared to individuals with only MDD (family
history of depression, low positive emotionality).
Further, the MDD-only group showed less severe
stressors than the comorbid MDD and GAD group,
whereas the GAD-only group did not, suggesting that
the presence of GAD may impart a greater risk for
severity despite common genotypic influences of the
disorders. Further, Kendler et al.  found that
types of life events differentially predicted MDD and
GAD (using a 2-week minimum duration) in 7,322
male and female twins from the Virginia Twin Registry.
Humiliation events predicted pure MDD, but not pure
GAD. In contrast, danger events predicted pure GAD,
but not MDD. However, most events characterized by
loss were nonspecific with the exception of death and
respondent-initiated separation from significant others,
which were specific for pure depressive episodes.
THE FUNCTIONAL RELATIONSHIP
BETWEEN GAD AND MDD
Given the differences in environmental stressors
between GAD and MDD, it is important to determine
when these disorders appear similar in emotional
characteristics and when they diverge over time.
Cuthbert  pointed out that it is unclear how
hierarchical models can discern mechanisms of change
in diagnostic phenomena over time from structural
data, which are static by definition (i.e., dispositional
emotionality). Brown  provided a notable excep-
tion to this assertion with an examination of structural
data over time using latent growth modeling to
determine the relationship between temperamental
stability and disorder influence over a 2-year period
in a clinical sample. Temporal covariation of GAD and
MDD was low (r5.30) and actually less than that of
social anxiety disorder and MDD (r5.54), suggesting
that these disorders do not occur largely in synchrony
over time. However, the temporal overlap between
GAD and MDD was explained primarly by their shared
relationship to negative affectivity. Further, initial
levels of negative affect accounted for a stable,
unremitting course in both GAD and MDD. Thus,
negative affectivity appears to play a role, yet cannot
fully account for, the temporal presentations of GAD
A focus on structural emotional vulnerability factors
may obscure functional relationships between emotional
phenomena in GAD and MDD. GAD typically onsets
earlier to the onset of an MDD episode, and the
presence of GAD increases the likelihood of a later
MDD episode to a greater degree than any other
anxiety disorder [see Kessler et al., 2004]. These results
suggest a possible functional relationship between
GAD and MDD, such that characteristics of GAD
may increase the likelihood of the characteristics of
MDD. Sole focus on the structure of emotion may
obscure the mechanisms by which emotional features
determine when someone expresses GAD versus MDD
or how, over time, GAD may lead to MDD. Indeed,
despite the high overlap in structural negative affect,
GAD and MDD appear to exhibit surprisingly distinct
patterns of emotional reactivity in laboratory settings.
In a review Rottenberg  had demonstrated that
individuals with a current episode of MDD are
characterized by a blunted emotional response to both
positive and negative emotional stimuli, which they
have termed context insensitivity to emotions. In
contrast, Mennin et al. [2005, study 3] and McLaughlin
et al.  have found hyperreactivity to various
emotional contexts in individuals with GAD. Thus,
although these disorders share an increased likelihood
for negative affect, they may be distinguished by
differences in shorter duration fluctuations in emo-
tional response as represented by either graded
(i.e., GAD) or flattened (i.e., MDD) peaks and valleys
in the overall landscape of their temporal emotion
presentation [Rottenberg, 2005]. Changes from heigh-
tened emotional reactivity to blunted emotional
response may provide a marker for mechanisms by
which GAD leads to an MDD episode. Possible
mechanisms for these changes in emotional reactivity
include functional changes from extreme goal focus to
motivational disengagement [see Johnson, 2005], from
uncertainty to certainty about the negativity of future
events [e.g., Dugas et al., 2004; Miranda and Mennin,
2007] or from beliefs of helplessness to beliefs of
hopelessness [see Alloy et al., 1990]. Delineation of the
role of emotion reactivity may not only elucidate
mechanisms through which GAD increases the like-
lihood of a subsequent episode of MDD but also help
inform the best approach to categorizing these
disorders (i.e., accounting for both structural overlap
and functional distinction) and, inevitably, inform
treatment of individuals suffering with both mood
and anxiety difficulties.
There have been numerous calls to restructure
classification of disorders in DSM-V [e.g., Watson,
296Mennin et al.
Depression and Anxiety
2005; Widiger and Clark, 2000]. Dimensional con-
structs such as neuroticism or negative affect account
for sizable portions of variance in the anxiety and mood
disorders and, thus, may provide a fruitful alternative to
the current nosological structure, which suffers from
poor distinctiveness among categories and high levels
of comorbidity. In particular, GAD and MDD demon-
strate significant overlap in genotype and phenotype
and relationships with higher-order negative affectivity
[see Watson 2005, 2008]. On the basis of these
findings, there have been a number of calls to reclassify
considerations to reclassify GAD should take into
account a number of factors related to GAD, MDD,
and their overlap with other anxiety and mood
disorders. First, GAD has established reliability and
validity in its own right, and specific features (e.g.,
worry) may be obscured by attempts at reclassification.
Second, examination of the overlap of GAD and MDD
with each other and with other disorders suggests a
more complex pattern of differences between these
conditions than has been suggested (e.g., MDD has
strong relationships with other anxiety disorders, and
GAD may be more strongly related to fear than it may
first appear). Third, although findings suggest that
GAD and MDD may have overlapping heritable
characteristics, other evidence suggests that the two
disorders may be distinguished by environmental
factors and temporal presentations. Further, whereas
dispositional overlap between GAD and MDD is
reflected in their relationships to negative affectity,
temporal relationships between these disorders may be
demonstrated by functional changes in emotional
These assertions suggest a more complex picture of
the relationship between anxiety and mood disorders
than suggested by Watson [2005, 2008]. Although
there is a clear need to consider dimensional classifica-
tion and the inclusion of higher-order emotionality
factors that reflect underlying genetic processes,
reliable differences support current distinctions in the
classification of specific mood and anxiety disorders.
One may see this issue as a classic ‘‘lumper’’ versus
‘‘splitter’’ debate with both approaches having merit.
However, it is difficult to determine how both general
and specific categories could be accounted for in DSM-
V. Watson [2005, 2008] and others [e.g., Krueger et al.,
1999] provide a compelling model for restructuring
classification to account for both higher-order char-
acteristics and lower-order category relationships.
However, given possible complexities in the overlap
of GAD and MDD with each other and with other
anxiety and mood disorders, alternative frameworks
deserve consideration. One possibility is that anxiety
and mood disorders could be diagnosed on three levels.
Rather than separating certain anxiety and mood
disorders or all anxiety and mood disorders from each
other, specific diagnoses of ‘‘emotional disorders’’
could be given at the lowest level of any of the existing
categories. At the next level, individuals could be
diagnosed according to positive or negative relation-
ships with structural emotional characteristic factors
such as negative affectivity (indicated by avoidance and
inhibition), positive affectivity (indicated by appetitive
and exploratory motivation), and physiological hyper-
arousal (indicated by heightened reactivity in auto-
nomic indicators). However, unlike Watson’s approach,
this level of diagnosis need not be orthogonal to lower-
order categories. In other words, positive affectivity
could relate negatively to both MDD and social anxiety
disorder; negative affectivity could relate positively to
MDD, GAD, and panic disorder [given findings from
Brown et al., 1998], and physiological hyperarousal
could positively indicate panic disorder and negatively
indicate GAD. At the highest level, one could also be
diagnosed solely by an internalizing factor, which
captures the overlapping relationships of all anxiety
and mood disorders. This system would also allow
examination of lower-order relationships within a
course of GAD and MDD in a sample of those
meeting criteria for ‘‘negative affectivity’’). Classifica-
tion changes in DSM-V will need to be empirically
evaluated, and changes that provide the greatest
amount of unique information are to be preferred.
Nonetheless, nosological changes to DSM-V that
simultaneously account for both overlap and distinc-
tiveness in disorders such as GAD and MDD may best
help advance our understanding of convergent and
divergent symptom presentations.
script thank Katie McLaughlin, Amelia Aldao, and
Michelle Blackmore for their intellectual contributions
to the ideas expressed in this paper. Portions of this
manuscript were presented at the Annual Satellite
Conference, Anxiety Disorders Association of America,
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299Is GAD an Anxiety or Mood Disorder?
Depression and Anxiety