Download The Role of Personality in Psychotherapy for Anxiety

The Role of Personality in Psychotherapy for Anxiety
and Depression
Richard E. Zinbarg,1 Amanda A. Uliaszek,2 and
Jonathan M. Adler2
1
Northwestern University and The Family Institute
at Northwestern University
2
Northwestern University
ABSTRACT A trait approach to personality has many implications for
psychotherapy. Given that traits contribute to the expression of symptoms of common psychiatric disorders, are moderately heritable, and relatively stable (yet also dynamic to some extent), long-term change in
symptoms is possible but is likely to be limited. Analogous to the manner
in which genes set the reaction range for phenotype, standing on certain
traits may set the patient’s ‘‘therapeutic range.’’ On the other hand, some
of the same traits that may limit the depth of therapeutic benefits might
also increase their breadth. In addition, taking the patient’s standing on
different traits into account can inform the choice of therapeutic strategy
and targets and can affect the formation of the therapeutic alliance and
compliance with self-help exercises. Finally, other aspects of personality
beyond traits, such as ego development and narrative identity, also appear to have important implications for psychotherapy.
A great deal of theory and research has focused on the implications
of personality traits for the development and course of psychopathology. Indeed, questions concerning the associations between personality traits and the development and course of psychopathology
were a central focus of the research programs developed by H. J.
Eysenck (e.g., 1967) and J. A. Gray (e.g., Gray & McNaughton,
Preparation of this article was supported by the Patricia M. Nielsen Research Chair of
the Family Institute at Northwestern University and by National Institutes of Health
Grant R01-MH65652-01 to Richard E. Zinbarg.
Correspondence concerning this article should be addressed to Richard Zinbarg,
Department of Psychology, Northwestern University, 2029 Sheridan Rd., Evanston,
IL 60208-2710; E-mail: [email protected].
Journal of Personality 76:6, December 2008
r 2008, Copyright the Authors
Journal compilation r 2008, Wiley Periodicals, Inc.
DOI: 10.1111/j.1467-6494.2008.00534.x
1650
Zinbarg, Uliaszek, & Adler
2000). Far less attention has been paid, however, to implications that
personality traits have for psychotherapy. Yet a trait approach to
personality has great potential to be useful in the psychological
clinic. In this article, we explore the implications of personality traits
for prognosis: choosing therapeutic strategies, identifying therapeutic targets, deciding whether medications are necessary, developing
the therapeutic alliance, and ensuring compliance with between-session practice/self-help exercises.
Our primary focus is on four questions regarding the nature of
personality traits and the relationship between personality traits and
psychopathology. Two considerations guided our selection of questions to focus on. First, we believe that, relative to other questions
we considered, these four questions either have more fundamental
implications for psychotherapy or have been mistakenly taken to
have such implications by laypeople and even experts in some cases.
Second, given our commitment to empirically informed psychotherapy, we also limited ourselves to questions for which personality
science has provided relatively firm answers.
The first, and most fundamental, of our four questions is ‘‘Do
personality traits contribute to the development, maintenance, and/
or expression of psychopathology?’’ If the answer to this question is
‘‘No,’’ then the implications of personality traits for psychotherapy
would seem to be limited to whether certain traits might influence the
therapeutic alliance or other aspects of the therapeutic process such
as patient compliance. On the other hand, if traits do contribute to
the development and/or maintenance of psychiatric symptoms, then
characteristics of traits such as their degree of mutability would seem
to be central to considerations of patient prognosis.
Our second question is ‘‘How stable are personality traits?’’
This question bears directly on mutability and therefore prognosis. For example, if traits contributing to symptoms are perfectly
stable, it would seem that prognosis would be rather grim in many
cases.
Our third question is ‘‘How heritable are personality traits?’’ As
one’s genotype is invariant, it is assumed by some patients whom we
work with—and perhaps by some therapists and researchers—that if
much of the reliable variance in traits contributing to symptoms is
heritable, then the prognosis for most psychotherapy cases would be
rather grim, whereas biological interventions stand a better chance
of working and are perhaps even necessary.
Personality Traits and Psychotherapy
1651
The final question we consider is ‘‘Are personality traits hierarchically structured?’’ If so, an important task confronting psychotherapists and their patients is to determine which levels of the
hierarchy are the most relevant for each aspect of treatment planning
and implementation.
In this article, we discuss the literatures bearing on the four questions posed above. After answering these questions, we discuss their
implications for psychotherapy including challenging what we believe are two commonly held myths about personality and psychotherapy: that trait vulnerability factors cannot be altered by
psychotherapy and that medications are necessary for symptom reduction. Given our expertise in anxiety and unipolar depressive disorders, almost all of our examples involve the treatment of these
disorders. Finally, we will also briefly consider psychotherapeutic
implications of aspects of personality beyond traits.
The current diagnostic system of the American Psychiatric Association posts several distinct acute clinical syndromes that are seen as
reflecting deviations from the individual’s usual functioning and collectively comprise the Axis I disorders. It is important to note that
according to this system, the Axis I disorders are distinct from personality disorders that collectively comprise the Axis II disorders
and are believed to be more chronic and encompass the individual’s
usual ways of interacting with the world. Given the distinct boundaries posited in the diagnostic system and that we focus only on the
treatment of Axis I internalizing disorders, it might be thought that
our hypotheses are necessarily limited to these disorders. Nonetheless, we believe that many of the hypotheses we discuss also apply to
other disorders, including many of the Axis II disorders. The reason
we say this is that empirical evidence exists that greatly blurs the
boundary between Axis I and Axis II. First, Axis I and Axis II disorders are highly co-occurring. Those with a Cluster B or Cluster C
personality disorder have a significantly greater chance of also having a mood or anxiety disorder (e.g., Coid, Yang, Tyrer, Roberts, &
Ullrich, 2006; Lenzenweger, 2006). Second, some mood and anxiety
disorders and Axis II disorders (particularly in Cluster C) share specific symptoms (e.g., social phobia and avoidant personality disorder, dysthymia, and depressive personality disorder), further
blurring
the
Axis
I-Axis
II
boundary
(Krueger,
2005). Third, mood and anxiety disorders are associated with the
same personality traits that characterize at least some personality
1652
Zinbarg, Uliaszek, & Adler
disorders (Widiger, 2003). Finally, Axis I and Axis II disorders are
not distinguishable in many important ways, including stability, age
of onset, degree of insight, or genetic versus psychosocial etiology
(e.g., Krueger, 2005; Widiger, 2003).
Treatment response may be one of the areas where there may be
important differences between Axis I and Axis II. Because there are
many more treatment studies of Axis I than Axis II, this continues to
be an area of debate (Beck, Freeman, & Davis, 2004; Krueger, 2005).
While several uncontrolled clinical reports and single-case design
studies yield positive results for cognitive-behavioral therapy across
9 of 10 personality disorders (excluding schizotypal), controlled
treatment studies seem to exist only for antisocial, avoidant, and
borderline personality disorder (Beck et al., 2004). These studies
have yielded mixed results; at worst, treatment results in little change
in symptomatology (e.g., those with antisocial personality disorder
who were not depressed; Luborsky, McLellan, Woody, O’Brien, &
Auerbach, 1985); at best, treatment results in a reduction of serious
symptoms (for example, in dialectical behavior therapy for borderline personality disorder; Linehan, Armstrong, Suarez, Allmon, &
Heard, 1991). Some researchers are particularly optimistic about
these results, especially those involving dialectical behavior therapy
for borderline personality disorder (Krueger, 2005; Livesley, 2004).
However, it is important to note that this therapy consists of 1 year
of intensive treatment (much longer than many treatments of Axis I
disorders) and often results in only moderate overall improvement,
as opposed to complete recovery or high end-state functioning that is
more commonly seen in treatments of anxiety (e.g., Borkovec &
Whisman, 1996) and depressive disorders (e.g., Jacobson et al.,
1996). Even though there appears to be a mean difference between
Axis I and Axis II disorders in treatment responses, however, the
many similarities between them suggest to us that the many of the
psychotherapeutic implications of traits we discuss will also apply to
Axis II disorders.
Four Basic Questions About the Nature of Personality Traits
Do personality traits contribute to the development, maintenance, and/
or expression of psychiatric disorders?
Several theorists have hypothesized a trait vulnerability factor common to most, if not all, of the internalizing disorders (e.g., Cloninger,
Personality Traits and Psychotherapy
1653
1986; Eysenck, 1967; Fowles, 1993; Gray & McNaughton, 2000;
Tellegen, 1985). This trait is defined slightly differently and given
different labels by different theorists—harm avoidance (Cloninger),
neuroticism (Eysenck), trait anxiety or behavioral inhibition system
sensitivity (Fowles, Gray) and negative affectivity (Tellegen). However, in our opinion, the conceptual and empirical overlap among
these conceptualizations far outweighs the differences, and a discussion of the subtle differences among these conceptualizations is beyond the scope of this article. Each of these conceptualizations
implies a trait disposition to experience negative affect. The term
neuroticism (N) will be used hereafter to acknowledge Eysenck’s pioneering work and to be consistent with the emergence of the Big
Five model of personality—which includes N, Introversion/Extraversion (I), Conscientiousness (C), Agreeableness (A), and Openness to experience (O)—as the dominant model of personality trait
structure (e.g., Goldberg, 1993; Watson, Clark, & Chmielewski,
2008).
In factor-analytic terminology, the hypothesis of a common risk
factor implies that there should be a general factor that is common to
depression and all of the anxiety disorders. Indeed, evidence for such a
general factor has consistently been obtained across samples seeking
psychiatric treatment (e.g., Zinbarg & Barlow, 1996), epidemiological
samples (e.g., Fergusson, Horwood, & Boden, 2006; Krueger, 1999;
Krueger, Caspi, Moffitt, & Silva, 1998; Vollebergh et al., 2001) and in
a large, multinational sample comprising consumers of general health
care service centers (Krueger, Chentsova-Dutton, Markon, Goldberg,
& Ormel, 2003). There is also evidence not only of a general factor in
cross-sectional analyses but also in longitudinal analyses (Ferguson
et al., 2006; also see Gregory et al., 2007).
Though the evidence regarding the general factor common to the
Axis I internalizing disorders is consistent with the hypothesis that
there is a risk factor common to all of these disorders, there is an
alternative explanation that these results are not capable of ruling
out. That is, it is possible that the second-order factor may have
arisen entirely as a consequence of demoralization resulting from
developing an internalizing disorder rather than from a variable of
etiologic significance (Frank, 1961; Link & Dohrenwend, 1980).
Evidence with some bearing on this alternative explanation has
come from multivariate, behavior-genetic studies conducted by
Kendler and his colleagues (e.g., Hettema, Prescott, Myers, Neale,
1654
Zinbarg, Uliaszek, & Adler
& Kendler, 2005; Kendler, Prescott, Myers, & Neale, 2003). These
results suggest strongly that a genetic factor is largely responsible for
the pattern of symptom covariance that results in the frequently cooccurring symptoms of internalizing disorders. Furthermore, it seems
likely that the genetic factor is at least partly, if not entirely, related to
the vulnerability to these disorders. Indeed, data we review next from
longitudinal studies demonstrate that N and related traits (e.g., behavioral inhibition and anxiety sensitivity) do prospectively predict
the onset of new episodes of MDD and anxiety disorders (for a more
detailed discussion of the studies on the phenotypic and genetic
structure of the internalizing disorders, see Zinbarg & Yoon, 2008).
Clark, Watson, and Mineka (1994) reviewed several longitudinal
studies showing N to be a predictor of both subsequent diagnoses
and chronicity of major depression. Since that review, studies reported by Hayward, Killen, Kraemer, and Taylor (2000), Kendler
and colleagues (e.g., Kendler, Kuhn, & Prescott, 2004), and Krueger,
Caspi, Moffitt, Silva, and McGee (1996) obtained results consistent
with the conclusions arrived at by Clark et al. (1994). Krueger et al.
also found that N is an especially good marker of risk for multiple
diagnoses of emotional disorders.
For anxiety disorders, Clark et al. (1994) also reviewed evidence
that N is a risk factor for the development of post-traumatic stress
disorder. Additional longitudinal studies have shown that children
high on behavioral inhibition (thought to be a precursor to, and
facet of, N; Turner, Beidel, & Wolff, 1996) are at greater risk for the
development of multiple phobias and other anxiety disorders in later
childhood (Biederman et al., 1990, 1993; Hirschfeld et al., 1992) and
social phobia in adolescence (Hayward, Killen, Kraemer, & Taylor,
1998; Schwartz, Snidman, & Kagan, 1999). Hayward et al. (2000)
also found N to be a predictor of panic attacks in a 4-year prospective study of adolescents. Thus, extant data are consistent with the
hypothesis that N is a marker of vulnerability for both major depression and anxiety disorders.
Other studies have focused on more narrow facets of N. For example, negative beliefs about the consequences of experiencing anxiety, known as anxiety sensitivity (AS; Reiss, 1980), are believed to
be facets of N that confer vulnerability for panic attacks and panic
disorder and, to a lesser degree, other anxiety disorders. Laboratory
studies supporting a role for AS in panic attacks entail panic provocation procedures. In nonclinical samples, AS predicts subjective
Personality Traits and Psychotherapy
1655
distress and reported symptomatology in response to CO2 inhalation
(Forsyth, Palav, & Duff, 1999), and hyperventilation (Sturges,
Goetsch, Ridley, & Whittal, 1998), even after partialing trait anxiety (Rapee & Medoro, 1994). Several longitudinal studies now indicate that AS is a marker of vulnerability for the onset of panic
attacks over 1- to 4-year intervals in adolescents (Hayward et al.,
2000), college students (e.g., Li & Zinbarg, 2007), and community
samples with specific phobias or no anxiety disorders (Ehlers, 1995).
In addition, AS predicted the development of worry about panic
(and anxiety more generally), during an acute military stressor (i.e., 5
weeks of basic training), even after partialing history of panic attacks
and trait anxiety (e.g., Schmidt et al., 1999). Finally, whereas the
clinical/practical importance of AS in symptom genesis has been
questioned based on small effect size estimates (Schmidt, Lerew, &
Jackson, 1999), Li and Zinbarg (2007) demonstrated that when AS is
measured properly (i.e., in accordance with its hierarchical structure)
it predicts meaningful proportions of variance in the onset of panic.
Given that low positive affect (PA) or anhedonia is relatively specific to depression (e.g., Clark & Watson, 1991), Fowles (1993) and
others hypothesized low positive emotionality (PEM) to be a traitvulnerability marker for depression. Despite different labels for this
marker— PEM (Tellegen, 1985) and Introversion (I; DePue & Iacono, 1989)—similarities in these conceptualizations, in our view,
outweigh the differences, and a discussion of the subtle differences
among these conceptualizations is beyond the scope of this article.
We will refer to this trait as I, again to acknowledge Eysenck’s
pioneering work and to be consistent with the Big Five model of
personality. Several longitudinal studies suggest that I is a predictor
of subsequent depressive symptoms (e.g., Levenson, Aldwin, Bosse,
& Spiro, 1988; Holahan & Moos, 1991) and diagnoses (Hirschfeld
et al., 1989; Krueger et al., 1996), but other studies did not replicate
these findings (e.g., Gershuny & Sher, 1988; Kendler et al., 1993).
Gershuny and Sher (1998) found that I interacted with N in the
prediction of symptoms of depression although Jorm et al. (2000)
failed to replicate this interactive effect. A more consistent finding is
that I has been shown to be positively associated with the chronicity
of the course of major depression (Clark et al., 1994). There is also
evidence that children at risk of depression by virtue of having a
mother with a history of depression are low on observational measures of PEM (Durbin, Klein, Hayden, Buckley, & Moerk, 2005).
1656
Zinbarg, Uliaszek, & Adler
Structural modeling studies have also been informative about the
relationship between normal and abnormal traits or characteristics.
O’Connor (2002) meta-analyzed dozens of correlation and factor
loading matrices published in English-language journals over the past
50 years. This included data on 37 measures, both normal (e.g., 16
Personality Factor Questionnaire, California Psychological Inventory) and abnormal (e.g., Beck Depression Inventory, MMPI) in content and with clinical and nonclinical populations. The results
indicated that the same number of components existed in the measures for both clinical and nonclinical populations, with the factor
structure looking essentially the same for the two groups. Another
study completed a meta-analysis on 77 samples from 52 studies
examining five different personality measures (Markon, Krueger, &
Watson, 2005). Markon, Krueger, and Watson (2005) also found an
integrated model of normal and abnormal personality, which they
then replicated in a sample of college-age participants. Thus, these
two meta-analyses converge in suggesting that psychopathology
symptoms can often be explained as extreme variants of normal traits.
Similar structural questions have been studied in the area of
personality disorders (PDs). O’Connor and Dyce (2001) reported a
five-factor structure of PDs. Importantly, normal and abnormal
personalities were distinguishable only by vector length, a measure
of rigidity, and extremity of the trait. Miller, Lynam, Widiger, and
Leukefeld (2001) also reported results that support the contention
that psychopathy can be understood as extreme standing on several
Big Five personality factors, most notably extremely low A and extremely low C. One possible exception to the conclusion that PD
symptoms can be explained as variants of normal traits is the evidence presented by Watson, Clark, and Chmielewski (2008) that
the Big Five needs to be expanded to incorporate a dimension—
Oddity—relevant for the symptoms related primarily to the Cluster
A PDs. On the other hand, Watson et al. (2008) also review evidence
that the Big Five personality factors (with the exception of Openness) provide an adequate basis for the assessment of the characteristics related to the Cluster B and Cluster C PDs.
In concluding this section, it is clear that N-related and I-related
traits are markers of mechanisms that contribute to the development
and/or maintenance of anxiety and depressive disorders. Whereas
there is a need for longitudinal research testing whether other traits
are markers for risk of other disorders, cross-sectional research on
Personality Traits and Psychotherapy
1657
structural models suggests that four of the five Big Five personality
factors (i.e., all but Openness) might contribute to the development,
maintenance, and/or expression of PDs.
How stable are traits?
McCrae and Costa (1996) concluded that much research has shown
that normal personality traits tend to remain relatively stable throughout a person’s lifetime. Consistent with this, a recent study by Watson
and Humrichouse (2006) found rank-order stability in the .7 range (with
little variability across different traits) for a 2-year interval for both selfand spouse ratings. Hampson and Goldberg (2006) found similar estimates of .70–.79 (.85–.98 corrected for unreliability) over 2.8 years in an
adult sample. Indeed, based on the observation that the asymptotic
values (as retest intervals lengthen) of adult trait temporal stability coefficients are above zero, Fraley and Roberts (2005) concluded that
there must be a constant factor contributing to trait scores over time.
At the same time, it is important to note that a well-accepted principle among researchers in this area is that the longer the retest interval, the lower the level of rank-order stability (e.g., Roberts &
DelVecchio, 2000). For example, Hampson and Goldberg also reported very modest temporal stability coefficients over a 40-year interval spanning elementary school and midlife including values of .16
for O, .08 for A, and .00 for N. Though it is almost certain that higher
values would have been obtained if the 40-year retest interval had
spanned early adulthood to older adulthood (e.g., Fraley & Roberts,
2005; Roberts & DelVecchio, 2000). Other studies have also demonstrated moderating variables that are associated with changes in personality, at least in the period of adolescence to young adulthood. For
example, the introduction of a controlled stressor (12-month exposure
to an intercultural environment) can decrease personality vulnerability in terms of trait anxiety, locus of control, and defensiveness (Andrews, Page, & Neilson, 1993). Another study showed that one’s work
experience, including success, power, satisfaction, and security in
young adulthood can modify basic personality dimensions, particularly N and E (Roberts, Caspi, & Moffitt, 2003). These results illustrate the point that personality traits, though relatively stable in the
short- and midterm, are far from immutable.
Results have consistently shown that N and I scores significantly
increase (sometimes up to one standard deviation) during a depres-
1658
Zinbarg, Uliaszek, & Adler
sive episode (see Costa, Bagby, Herbst, & McCrae, 2005; Ormel,
Oldehinkel, & Vollebergh, 2004; Santor, Bagby, & Joffe, 1997). This
has caused much confusion and controversy among personality
researchers, with some concluding that personality measures are
systematically biased by acute depression, therefore questioning the
validity and usefulness of personality assessment during depressive
episodes (e.g., Hirschfeld, Klerman, Clayton, & Keller, 1983). Other
researchers have proposed that it is erroneous to believe that personality traits are immutable but that the changes in trait scores that
occur during a depressive episode represents a ‘‘true’’ change in personality (Costa et al., 2005). Widiger and Trull (1992) discuss a third
possibility of a spectrum relationship in which both personality and
disorder stem from common causes and vary together.
While this debate is not yet settled, sophisticated methodological
techniques may make it possible to do so in the future. Thus, a study
might use informant reporting to rule out the possibility that reporting bias is entirely responsible for the changes in trait scores
during a depressive episode. Of course, it is possible that the observed changes reflect both reporting bias and true trait or spectrum
change. Teasing apart the trait change and spectrum change explanations is probably more challenging, and a full discussion of this
issue is beyond the scope of this article. Briefly, though, the crux of
the difference seems to be that the trait change explanation implies
that N and depressive episodes are related yet distinct constructs,
whereas the spectrum explanation implies that although they reflect
a single trait, they reflect different location parameters along this
trait. Thus, one could use confirmatory factor analysis for categorical items—equivalent to multidimensional Item Response Theory
analysis (e.g., Muthen, 1984; Takane & de Leeuw, 1987—to test
whether a diagnosis of depression and symptoms of depression define a separable factor from that defined by items tapping N. Certainly, regardless of how this debate is ultimately resolved, the
evidence regarding changes in trait scores associated with depressive episodes is consistent with the conclusion based on trait stability
studies in nonclinical samples that traits are not immutable.
How heritable are traits?
Behavioral genetic research has yielded consistent results indicating
a moderate heritable component of traits. There appears to be little
Personality Traits and Psychotherapy
1659
differential heritability across traits with estimates falling in the
moderate range of .20 to .60 (e.g., Jang, McCrae, Angleitner, Riemann, & Livesley, 1998; Keller, Coventry, Heath, & Martin, 2005;
Loehlin, Neiderhiser, & Reiss, 2003; Saudino & Plomin, 1996).
Shared environment (e.g., parenting style, socioeconomic status,
neighborhood) accounts for, at most, a small portion of variance
in most traits (e.g., McCrae, Jang, Livesley, Riemann, & Angleitner,
2001; Saudino, Plomin, & Defries, 1996). However, some studies
have found that larger shared environmental effects are sometimes
found when variables that moderate heritability are modeled (Krueger, South, Johnson, & Iacono, this issue). Nonshared environmental effects (e.g., peer group influence, birth order effects, accidents,
illnesses) for personality traits are estimated to fall between .4 to .8
(e.g., Saudino & Plomin, 1996). It is important to remember that
nonshared environment is computed as a residual score, which includes the variance, if any, associated with the interaction of the genotype by shared environment, systematic method variance, random
error variance, and nonadditive genetic effects.
Also, pertinent to this discussion is the heritability of psychopathology, with a focus on depressive and anxiety disorders. Research
has shown that major depressive disorder (MDD) has a heritability
estimate of approximately .4–.5, with the remaining variance
accounted for by nonshared environmental effects (for review, see
Levinson, 2005; Sullivan, Neale, & Kendler, 2000). Behavioral genetic analyses of anxiety disorders yield similar results, with estimates of heritability generally ranging from .3–.4 (see Hettema,
Neale, & Kendler, 2001). Again, common environmental effects were
nil, with nonshared environmental effects accounting for 60–70% of
the variance. As mentioned above, multivariate behavior-genetic
studies suggest at least one genetic factor common to MDD and the
anxiety disorders (e.g., Hettema et al., 2005; Hettema, Neale, Myers,
Prescott, & Kendler, 2006; Kendler et al., 2003). Moreover, N
appears to be related to one of these common genetic factors (e.g.,
Hettema et al., 2006). For example, the association between N and
MDD results largely from shared genetic factors; approximately
50% of the genetic effects on MDD are shared with N (Kendler,
Gatz, Gardner, & Pedersen, 2006). For GAD, this number is approximately 35% (MacKintosh et al., 2006).
Behavioral genetic research not only studies the variance
accounted for by genetics and the environment within traits, but
1660
Zinbarg, Uliaszek, & Adler
the covariation between traits. Multivariate factor analyses have
been completed on genetic correlations of groups of traits, leading
behavioral genetic research to support two-, three-, four-, and fivefactor models of personality (Krueger & Johnson, 2007). This
research also supports personality structure at the individual facet
level beneath the Big Five ( Jang et al., 1998). Taken together, this
evidence suggests that genetic influences on personality traits are not
confined to one specific level of the personality hierarchy but affect
the entire hierarchy and all of its levels. The phenotypic structure of
personality traits, as discussed below, appears to mirror this hierarchical organization (Krueger & Johnson, 2007).
Are personality traits hierarchically structured?
As noted earlier, the dominant model of normal personality trait
structure is the Big Five (e.g., Goldberg, 1993). Many theorists have
represented and emphasized the hierarchical structure of the Big
Five (e.g., Costa & McCrae, 1997; Digman, 1997; Eysenck, 1947;
Watson et al., 2008). Importantly, though different researchers have
endorsed what might appear to be different structural models, Markon, Krueger and Watson (2005) present evidence that the structures
put forward by these different theorists can be integrated and understood as focusing on different levels of the same hierarchical
structure. Costa and McCrae (1997) present the Big Five at the
highest level of the hierarchy, with each Big Five factor comprised of
six lower order facets. Digman (1997) presents a five-level hierarchy
with the fourth level consisting of the Big Five, with two additional
factors, a (comprised of A, N, and C) and b (comprised of O and I),
at Level 5. Levels 1–3 in the Digman model are those proposed by
Eysenck (1947): Level 3 is facets of the Big Five, Level 2 is habitual
responses, and Level 1 is specific responses to situational cues.
Eysenck (1992) advocated that Level 4 (represented by the Big
Five in Digman’s model) consists of only three factors: I, N, and
psychoticism (P). In Eysenck’s model, A and C reside on Level 3, as
facets of P.
Based on both theory (e.g., Lilienfeld, Turner, & Jacob, 1993) and
empirical evidence (e.g., McNally, 1996; Zinbarg & Barlow, 1996;
Zinbarg, Barlow, & Brown, 1997; Zinbarg, Brown, Barlow, &
Rapee, 2001), we view N-spectrum traits as comprising a four-tiered
hierarchy with N as a fourth-order trait that is related to the general
Personality Traits and Psychotherapy
1661
tendency to react with negative affect to stressful stimuli. (It is worth
noting, however, that we agree with Livesley, 2007, that we see no
reason why nature should be ordered so neatly that all five Big Five
traits comprise structures with the same numbers of levels or the
same number of facets per level.) Trait anxiety is a third-order facet
of N related to the slightly less general tendency to react anxiously to
potentially threatening stimuli (with trait depression and hostility
being examples of other third-order facets of N). AS is a secondorder facet (perhaps corresponding to Eysenck’s habitual response
level) of trait anxiety related to the more specific tendency to react
anxiously to one’s own anxiety. Finally, AS is divisible into three
first-order facets (corresponding to Eysenck’s level of specific responses to particular cues) relating to concerns about different domains: (a) AS-Physical Concerns (fear of the physical sensations of
anxiety related to the belief that they will result in physical catastrophe), (b) AS-Mental Incapacitation Concerns (fear of the mental
and emotional manifestations of anxiety related to the belief that
they will result in emotional catastrophe), (c) AS-Social Concerns
(fear of publicly observable sensations of anxiety related to the belief
that they will result in social catastrophe). Whereas AS tends to be
elevated in all anxiety disorders and major depression, profiles across
the first-order facets of AS appear to be useful for discriminating
among these disorders (Zinbarg et al., 1997).
Hierarchical models are important for studying personality
and related constructs, partly because of the ‘‘bandwidth/fidelity
trade-off ’’ (Cronbach & Gleser, 1957). This refers to the notion that
broad constructs (those at the top of a hierarchy) are useful in
predicting diverse behaviors at moderate levels of accuracy, while
narrow constructs (those at the bottom of a hierarchy) are useful at
predicting a limited range of behaviors at a high level of accuracy.
This might imply that a personality construct should ideally be
studied at different levels of breadth (Hampson, John, & Goldberg,
1986). However, some researchers have identified a ‘‘basic level’’ of
personality traits, which they considered to be the most useful and
informative level. In a study by John, Hampson, and Goldberg
(1991) this level consisted of the highest level of the hierarchy that is
still behaviorally descriptive, the third level of a four-level hierarchy.
This level was preferred by John and colleagues over the more abstract superordinate levels and the more basic and specific subordinate levels, illustrating a good compromise between bandwidth
1662
Zinbarg, Uliaszek, & Adler
and fidelity. When it comes to implications for psychotherapy, however, it seems to us that different levels of the hierarchy each have
their own contributions to make. Our discussion of treatment
planning to follow draws heavily on the second and first levels. In
contrast, our discussion of the breadth of therapeutic benefits is most
germane to the third and fourth levels.
Myths Based on the Evidence Bearing on One or More of the Four
Basic Questions About the Nature of Personality Traits
Trait vulnerability factors cannot be altered by psychotherapy
Some researchers seem to have either implicitly or explicitly assumed
that trait vulnerability factors cannot be altered by psychotherapy.
For example, Mathews, Mogg, Kentish, and M. Eysenck (1995)
suggest that their finding that cognitive-behavioral therapy (CBT)
for generalized anxiety disorder (GAD) reduced an information
processing bias is ‘‘consistent with two alternative views: either that
cognitive bias depends on current state factors such as mood, or that
vigilance represents an enduring characteristic that becomes apparent only when vulnerable Ss are under stress’’ (p. 302). Clearly, an
implicit assumption underlying this argument is that trait vulnerabilities can’t be altered by psychotherapy (ergo, any characteristic,
such as an information-processing bias, which appears to have been
altered by therapy must neither be a trait vulnerability factor nor
have been altered but rather is one not currently being expressed). In
turn, this implicit assumption seems likely to stem from thinking of
traits as being immutable. Notably absent from this discussion is the
possibility that threat-processing biases are trait vulnerability markers that are relatively enduring but not immutable and that, therefore, are at least partly modifiable by experiences such as therapy. In
contrast, the literature cited above clearly shows that traits can be
vulnerability factors that are relatively enduring but far from immutable. Given the mutability of traits, we believe they can be modified to some degree by therapy.
Consistent with our belief, there are several studies that have provided evidence for a change in personality trait scores over the course
of therapy, with most concentrating on the Big Five traits over the
course of treatment for depression (e.g., Clark, Vittengl, Kraft, &
Jarrett, 2003; De Fruyt, Van Leeuwen, Bagby, Rolland, & Rouillon,
Personality Traits and Psychotherapy
1663
2006; Du, Bakish, Ravindran, & Hrdina, 2002). As mentioned earlier, the major finding is that N and I scores tend to decrease over the
course of treatment for depression. This has been supported regardless of whether the treatment is psychotherapy (Clark et al., 2003) or
psychotropic medication (Bagby, Levitan, Kennedy, Levitt, & Joffe,
1999; Costa et al., 2005; Du et al., 2002; Santor et al., 1997). Moreover, whereas most of the medication studies failed to include the use
of a placebo control group, we are aware of at least one exception
that did find greater personality change associated with the active
medication than with a placebo (Tang, DeRubeis, Hollon, Shelton,
& Schalet, in preparation).
The basic effect, that of the change in N and I scores, is fairly
consistent among studies (although De Fruyt et al., 2006, found
only a change in N), and there are two other important findings from
this body of research. First, though some studies have noted
that change in personality traits is correlated with change in depression (e.g., Clark et al., 2003; Du et al., 2002), other studies have
found that personality trait change occurs largely independent of
change in depression. From these studies we might conclude that
treatment for depression can have a significant effect on personality
traits, independent of the effect the treatment has on depression
(De Fruyt et al., 2006; Santor et al., 1997; Tang et al., in preparation). Second, studies have also demonstrated that personality trait
variables not only demonstrate absolute change in the form of
decreasing N and I but also rank order stability (De Fruyt et al.,
2006; Santor et al., 1997). We interpret these results to imply
that (a) the rank order stability found in these studies reflects
a constant source of variance in personality traits that
remains unchanged throughout adulthood (see Fraley & Roberts,
2005), and (b) the absolute change in personality trait measures seen
throughout depression treatment represents an actual altering of the
traits of N and I (for an alternative view, see Clark et al., 2003).
Medications are necessary for symptom reduction
Some of our patients (and according to their accounts, some of their
psychiatrists and former psychotherapists) hold the belief that the
heritability of traits likely involved in the development, maintenance,
and/or expression of common psychiatric disorders implies that medications are necessary for successful treatment. A simple version of
1664
Zinbarg, Uliaszek, & Adler
this argument might go something like this: if there is a biological
basis to psychopathology, then effective treatment must also involve
a biological intervention. A more sophisticated version might recognize that traits associated with symptoms are not immutable but assume that the genetic influences on these traits are and will continue
to produce symptoms if not addressed directly (i.e., biologically). Indeed, it is certainly true that the genotype remains constant over the
lifespan and will not be altered by psychotherapy. Yet both
versions of this argument are fallacious for four reasons.
First, heritability estimates are far from perfect. Thus, the environment clearly does influence traits even if the shared environment
does not.
Second, despite the fact that genotype remains constant over the
life span, heritability estimates can, and sometimes do, change as a
function of age perhaps due to variability in gene expression over
time and/or to gene-environment transactional processes (e.g.,
McGue, Bouchard, Iacono, & Lykken, 1993; Plomin & Spinath,
2004). Similarly, estimates of the influence of the shared, familial
environment can, and sometimes do, change as a function of age
probably due to the potency of more recent environment influences
relative to more distal environmental influences (McGue et al., 1993;
Plomin & Spinath, 2004). That is, genetic influences are clearly not
constant over time.
Third, heritability estimates are specific to the range of environments represented in the samples they are based on. Even if the range
of sampled environments is large, heritability estimates still only
represent an average of these without any information regarding
the effect of a specific environment. For example, Krueger and
colleagues (this issue) found that genetic shared environmental and
nonshared environmental effects were moderated by the participants
perception of their parental relationship. That is, when participants
rated the relationship low in Regard, this diminished genetic effect
and enhanced nonshared environmental effects. When participants
rated the relationship high in Conflict, this diminished the genetic
effect and enhanced shared environmental effects. It is possible that
with further advances in psychotherapeutic theory and technique
that psychotherapies for some conditions will represent systematic
environmental perturbations larger than any represented in extant
behavioral genetic studies and large enough to lead to larger trait
differences than those obtained to date.
Personality Traits and Psychotherapy
1665
Finally, we know that experience changes the structure of the
brain (e.g., Merzenich, 1998). Thus, psychotherapy is capable of
leading to brain reorganization such that medications are not
necessary even to effect changes in the biological bases of traits.
Psychotherapeutic Implications of the Research Bearing on the
Four Basic Questions About the Nature of Personality Traits
If the basic research findings concerning the nature of traits does
not support the inferences that trait vulnerability factors cannot be
altered by psychotherapy or that medication is necessary, what
then are the implications of this research? We next turn our attention to some of the implications that we believe traits can have for
psychotherapy.
Prognosis: The depth of psychotherapeutic benefits
Given that personality traits such as N, AS, and I appear to be involved in the development or maintenance of symptoms, the patient’s standing on these traits may place constraints either on the
amount of therapeutic improvement he or she might experience or
on the durability of such improvements. Indeed, if these traits had
been shown to be entirely heritable and perfectly temporally stable in
test-retest studies, then it might seem reasonable to argue that the
benefits of psychotherapy would be fleeting at best. Even then, however, if few participants in the studies producing the perfect heritability and stability coefficients had been in psychotherapy, such an
argument would not be unassailable. Fortunately, we do not need to
debate such issues as it is clear that traits are not immutable given
that they are neither completely stable nor entirely heritable. Thus,
whereas some might argue that if traits are involved in symptom
development, maintenance, and/or expression then long-term
change in symptoms as a result of psychotherapy would be impossible, such a view is clearly not warranted by the evidence. That is,
given that traits are not immutable, the fact that there are trait influences on symptom development, maintenance, and/or expression
certainly does not imply that long-term change in symptoms should
be impossible.
What then are the psychotherapeutic implications of the findings
that personality traits are partially heritable and of those that led
1666
Zinbarg, Uliaszek, & Adler
Fraley and Roberts (2005) to conclude that there is a factor (i.e.,
one’s genotype) that provides a constant contribution to variance in
personality traits? These findings are certainly consistent with our
belief that the benefits of psychotherapy are likely to be at least
somewhat limited in magnitude both in terms of effects on symptoms
and on traits (for a related discussion, see Harkness & Lilienfeld,
1997). That is, the evidence suggests that there is a limit to the benefits of even the most effective of our currently available treatments.
For example, in a trial of CBT for GAD Zinbarg, Lee, and Yoon
(2007) obtained large effect sizes (on average symptom scores at
post-test in the treatment group were 1.48 standard deviations (SDs)
lower than in the wait-list group and 1.71 SDs lower than their own
pretest scores). Despite these statistically large effects, the clinical
significance of the findings were much more limited. Only 50% of the
patients achieved high end-state functioning (i.e., being brought
within 1 SD of the normal mean) on four of five outcome measures,
and we are not aware of any studies that have obtained meaningfully
better high-end state functioning results with GAD. Moreover, consistent with the findings cited above that whereas N and I tend to
decrease during treatment they often remain elevated relative to the
normal population (Costa et al., 2005; De Fruyt et al., 2006; Du
et al., 2002), none of the patients scored more than a half of a SD
below the normal mean on at least four of the measures.
Thus, it is possible to bring patients who begin therapy with
symptom scores outside of the normal distributions back into the
normal range as a result of therapy. We also believe it is possible to
improve on our current therapies such that even higher proportions
of our patients might achieve this high end-state functioning status in
the future. However, we do not think it is realistic to expect to bring
many high N patients to the low end of either symptom distributions
or the N distribution as a result of psychotherapy. In an analogous
fashion to the manner in which genes set the ‘‘reaction range’’
(Gottesman, 1963) for phenotype, we offer the speculation that
standing on a trait such as N may be said to set the patient’s
‘‘therapeutic range.’’
A weak version of the ‘‘therapeutic range’’ hypothesis does not
necessarily predict that pretreatment personality predicts the amount
of improvement a patient experiences. Rather, it may be that most
patients will begin therapy with high enough elevations on N
(or other relevant traits) that they all have a somewhat restricted
Personality Traits and Psychotherapy
1667
‘‘therapeutic range’’ and/or a restricted statistical range of trait
scores. (That is, it may be that there is an asymptotic function
between N and ‘‘therapeutic range’’ such that further increases in N
above some threshold value are not associated with further decreases
in ‘‘therapeutic range.’’) Thus, a weak version merely predicts that
very few patients will ever be brought more than approximately a
half of a SD below the normal mean on a majority of outcome
measures.
Interestingly, however, some (though certainly not all) studies
have shown that pretreatment personality traits have an impact on
treatment outcome consistent with a stronger version of the ‘‘therapeutic range’’ hypothesis. For example, some researchers have explored the role of one facet of N—perfectionism—as measured by
the Dysfunctional Attitudes Scale (DAS; Weissman & Beck, 1978) in
the Treatment of Depression Collaborative Research Program
(TDCRP). Over the course of treatment, patients with high to moderate levels of perfectionism at pretreatment made no significant
therapeutic gain after the eighth treatment session (Blatt & Zuroff,
2005). Using video recordings of a sampling of treatment sessions
and a measure that codes therapist and patient participation in the
therapeutic alliance (Krupnick et al., 1996), results indicated that
perfectionist patients showed a disengagement in therapy after the
eighth treatment session (Shahar, Blatt, Zuroff, Krupnick, & Sotsky,
2004; Zuroff et al., 2000). One possible explanation of these results is
that these patients may have tended to apply their perfectionistic
beliefs to the therapy, which would be certainly be consistent with a
trait perspective. If so, and if this tendency to apply perfectionistic
standards to their work in therapy were not treated directly, it would
have left the patients vulnerable to feeling they were ‘‘failing’’ in
therapy and hopeless. Hopelessness about therapy, in turn, would be
expected to lead to disengagement (but see Shahar et al., 2004, for an
alternative explanation).
Some might argue that the nonzero heritability estimates of personality traits and the tendency for temporal stability coefficients to
asymptote at values above zero (as the follow-up interval increases)
necessarily dictates that the upper limit to therapeutic benefit must
fall short of bringing patients to the low end of symptom and traitrisk factor distributions. If so, we believe such an argument would be
just as logically fallacious—and for many of the same reasons—as
the arguments that traits cannot be altered by psychotherapy or that
1668
Zinbarg, Uliaszek, & Adler
medications are necessary. Also, as in an example provided by
Hampson and Goldberg (2006) of the number of hair follicles per
square centimeter of scalp in men, characteristics with even higher
heritabilities than personality traits undergo radical changes. That is,
if men with genetically determined ‘‘thick’’ hair can, and sometimes
do, go bald, then genetic influences on traits do not preclude radical
change in standing on a trait. Thus, though we believe bringing
patients to the low end of symptom and trait-risk factor distributions
is unlikely, it is not logically impossible.
To summarize, we believe it is logically fallacious to argue
against the possibility of therapy leading to radical change in
personality traits based on evidence of their temporal stability and
heritability. At the same time, we believe that until good evidence for
such radical transformation is presented, it is best (and certainly
most realistic) for patients and therapists alike to set more modest
expectations for therapy given that many of the traits that contribute
to seeking psychotherapy in the first place may limit a patient’s
‘‘therapeutic range.’’
Prognosis: The breadth of psychotherapeutic benefits
Despite the limits to the depth of change we can realistically expect
from psychotherapy, we believe the personality trait literature gives
us more reason to be optimistic about the breadth of change. That is,
the fact that there appear to be broad risk factors that confer risk for
many forms of psychopathology offers some hope that when therapy
is beneficial, it might have broad effects beyond the specifically targeted symptoms. To the extent that psychotherapy focused on the
principal diagnosis leads to some reduction in one of those broad
factors, then we should expect improvement in comorbid conditions
even if they are not explicitly targeted in treatment.
To illustrate this point, consider the case of N and internalizing disorders. As discussed above, N appears to be a broad risk
factor for MDD and the anxiety disorders. Thus, psychotherapy
for any one of these disorders that produces change in one or more
the processes (e.g., biases in the processing of threatening and/or
ambiguous information, physiological hyper-reactivity, avoidance
behaviors) that likely link N to symptoms should also be associated
with reductions in symptoms of comorbid anxiety disorders or
MDD that aren’t explicitly targeted in the therapy. Indeed, whereas
Personality Traits and Psychotherapy
1669
there is a need for more research on the impact of psychotherapy
on comorbid conditions, the available evidence in the literature
on CBT for anxiety disorders supports the expectation of broad
improvement that extends to comorbid conditions not explicitly
targeted in therapy (Borkovec, Abel, & Newman, 1995; Brown &
Barlow, 1992).
Therapeutic strategy and targets
The bandwidth/fidelity trade-off may have specific implications in
the clinical setting, especially in terms of treatment planning. First,
personality trait measures can identify higher order traits that are
related to a wide range of thoughts, feelings, and behaviors that may
be causing distress in the patient (e.g., high N and high I) or that
might interfere with treatment (e.g., low C, low or extremely high A).
They give the therapist a broad, general view of how a patient thinks,
feels, and behaves. The therapist now has a starting point from
which to begin to understand the patient, develop strategies for
building a strong alliance, and think of possible interventions that
will be useful. For example, a therapist should be wary of a highly
agreeable patient for signs of false enthusiasm or possible alliance
tears that the patient does not verbalize because he or she is overly
motivated to please the therapist (Miller, 1991; Muten, 1991). Similarly, a therapist should be prepared to be highly reinforcing of a
low-conscientious patient for homework completion. However, specific treatment planning based solely on the higher order traits may
be unwise; closer examination of lower order facets will predict patients’ behaviors with higher accuracy, allowing for a more specific
treatment plan. Therefore, a second step involves examination of
lower order facets to more specifically tailor a therapeutic approach.
The lower order facets that comprise a higher order factor are often
distinct enough in kind to warrant different treatment approaches.
In other instances, lower order facets may not be this distinct but
may be distinct enough to inform the choice of the specific target that
a treatment approach is applied to. In general, it is likely that a person scoring high on one facet of a higher order factor will score high
on the rest. A closer examination of the facets, however, may reveal
informative data about the specific patient.
Let us also take the example of Introversion. A therapist with two
patients who are extremely introverted might deem them both to be
1670
Zinbarg, Uliaszek, & Adler
better candidates for individual therapy than for group therapy (especially if the therapy group were relatively unstructured, in which
case their participation would be expected to be minimal; for a related discussion see Miller, 1991). Consistent with this, Ogrodniczuk,
Piper, Joyce, McCallum, and Rosie (2003) found that I and N were
related to poor outcome in outpatient group therapy, whereas O and
A were related to good outcome. However, each patient might have
a distinct I facet profile that is informative to treatment planning.
For example, Patient #1 is especially low on the I facets of warmth
and gregariousness but average on the I facet of trait positive
emotionality. In contrast to his average standing on trait positive
emotionality, however, he is especially low on a measure of current
state positive emotions, indicating an anhedonic depressive state in
an individual who has at least average capacity for pleasure. A
treatment plan might focus on behavioral activation (e.g., Martell,
Addis, & Jacobson, 2001). On the other hand, Patient #2 is especially
low on the I facets of assertiveness and excitement seeking, indicating that this person avoids situations that might involve
increased emotional arousal, even if the end result is potentially
rewarding. A treatment plan might focus on assertiveness training
and behavioral exposures to increase tolerance of emotional arousal.
Another example involves N. A therapist, noting that there are
two patients high on the higher order trait of N, might first hypothesize that these people are especially likely to have a mood or anxiety
disorder, be prone to experiencing negative affect, and might benefit
from CBT. However, closer examination of their N facet profiles
may indicate that different therapeutic approaches are necessary.
Patient #3 is especially elevated on the anxiety and self-consciousness
facets, indicating that cognitive restructuring and behavioral exposures should be aimed at fear of evaluation. Patient #4 is especially
elevated on the impulsiveness and angry hostility facets, indicating
that relaxation training and anger management training might
be helpful.
A third example involves simultaneous consideration of I facets
and N facets. Patients #5 and #6 are both high on N, with especially
high elevations on the anxiety facet, thereby suggesting that exposure therapy may be beneficial. Patient #5 has at least average scores
on the I facet of PEM, whereas Patient #6 is low on the I facet of
PEM. Thus, one might be able to facilitate the exposure therapy
for Patient #5 with motivation interviewing techniques designed
Personality Traits and Psychotherapy
1671
to increase approach motivation for exposures (Zinbarg, 1998). In
contrast, such an approach might be of more limited value for
Patient #6, and the therapist should instead focus primarily on
decreasing avoidance motivation via cognitive restructuring to
facilitate the exposure therapy.
A fourth example involves the second-order and first-order facets
in our four-tiered N hierarchy. Patients #7 and #8 are both high not
only on the fourth-order trait of N but are also both high on the
third-order facet of anxiety. Thus, they would both be likely to benefit from CBT including exposure therapy. However, Patient #7 is
also high on the second-order facet of AS and the first-order facet of
AS-Physical Concerns, whereas Patient #8 is not. Rather, in addition
to an elevation on the third-order facet of trait anxiety, Patient #8 is
also high on the second-order facet of Specific Fears and the firstorder facet of Fear of Heights. Thus, exposure would be indicated
for both patients, but for Patient #7 we would recommend interoceptive exposure whereas we would obviously recommend either in
vivo or virtual exposure to heights for Patient #8 (see Zinbarg et al.,
1997). From these oversimplified examples, one can see how an
understanding of the hierarchical structure of personality and utilization of personality measures that take this structure into account
can be helpful for treatment planning.
Alliance
There is evidence that even in CBT, which emphasizes specific therapeutic techniques and deemphasizes the importance of the therapeutic relationship relative to many other schools of psychotherapy,
the strength of the therapeutic alliance is a predictor of outcome
(e.g., Castonguay et al., 1996; Klein et al., 2003; Krupnick et al.,
1996; Loeb et al., 2005). Thus, the patient’s standing on A might be
expected to predict outcome as mediated by its impact on the
therapeutic alliance (Miller, 1991). Consistent with this hypothesis,
Gurtman (1996) found that the patient’s standing on hostile-dominance predicts poor therapeutic alliance and outcome. This association might be moderated, however, by therapist skill at working
with disagreeable patients or by amount of attention to alliance
building paid by the therapist. That is, disagreeable patients should
require greater interpersonal skill, greater skill at repairing alliance
ruptures, and/or effort on the part of the therapist to achieve the
1672
Zinbarg, Uliaszek, & Adler
same level of benefit compared with agreeable patients with equally
severe initial symptoms.
Compliance
The best available evidence suggests that compliance with self-help
exercises in between sessions is a predictor of outcome in CBT (e.g.,
Addis & Jacobson, 2000; Burns & Spangler, 2000; Kazantis, Deane,
& Ronan, 2000). Thus, the patient’s standing on C, A, and O at
initial assessment might be expected to predict outcome as mediated
by compliance with self-help exercises (Miller, 1991). Knowledge of a
patient’s C level could be useful to a therapist in order to build in
extra structure when negotiating self-help exercises with a low C
patient (negotiating not only what exercises the patient will work on
between sessions but also when and what external cues will be used
to remind the patient when it is time to work on a given exercise).
Note that we use the verb negotiating rather than assigning; we believe it is always best practice to adopt a collaborative stance and
offer a menu of choices when it comes to self-help exercises. Knowledge of a patient’s A level could be helpful, however, to encourage a
therapist to be particularly mindful of these principles from the
outset of therapy with a highly disagreeable patient (Miller, 1991).
Finally, as most self-help exercises will involve the patient experimenting with behaviors, cognitions, or feelings, O may also be related to compliance (McCrae, 1991; Miller, 1991). Thus, knowledge
of a patient’s O level could help a therapist adopt a more incremental
approach to negotiating self-help exercises to gradually build up to
responses that deviate more and more from the patient’s usual repertoire.
Beyond Traits
It is worth mentioning that there are components of personality beyond traits that have important implications for psychotherapy. One
increasingly influential theory of personality suggests that traits form
the foundation or ‘‘dispositional signature’’ of personality (McAdams, 1995, p. 372), onto which are added two other distinct levels of personality: characteristic adaptations and narrative identity
(e.g., McAdams, 1995, 2001; McAdams & Pals, 2006). Characteristic
adaptations include a wide range of dynamic motivational, socialcognitive, and developmental aspects of human individuality. These
Personality Traits and Psychotherapy
1673
components of personality are contextualized within situations and
evolve over time. In addition, people vary with respect to the life
stories that they construct to provide their lives with a sense of unity
and purpose and to make meaning out of their experiences, a level of
personality termed narrative identity (e.g., McAdams, 1995, 2001;
Singer, 2004). These three levels of personality are sometimes related
to each other in predictable ways, and sometimes they are not, suggesting that characteristic adaptations and narrative identity are not
simply emergent properties of traits (e.g., McAdams, 1995; McAdams & Pals, 2006). Individual differences at each of these additional levels of personality have also been studied in relation to psychotherapy. Indeed, Singer (2005), adopting and expanding upon
this three-level approach to personality, strongly advocates that taking all components of personality into account, what he calls an
‘‘integrative, person based personality psychology, forms a scientific
and ethical basis for the treatment of individuals in psychotherapy’’
(p. 158). Westen, Gabbard, and Blagov (2006) echo this assertion in
their claim that a multileveled conception of personality structure
should serve as a context for understanding psychopathology and
therefore treatment. A comprehensive overview of these literatures is
well beyond the scope of the present article, but for completeness it is
important to acknowledge certain key findings that incorporate these
other levels of personality.
Characteristic adaptations–Ego development
One characteristic adaptation that has implications for psychotherapy is ego development (ED). ED is a life span developmental construct that concerns the complexity individuals use when making
meaning out of their experiences (e.g., Loevinger, 1976; Westenberg
& Block, 1993). Individuals’ stage of ED does not tend to show
strong correlation with their profile of dispositional traits, although
ED is sometimes observed to correlate with the trait of Openness
(Westenberg & Block, 1993). We have selected ED as an example
because it is an important, if sometimes overlooked, characteristic
adaptation among those that have been operationalized well for systematic empirical study (Westen, Gabbard, & Blagov, 2006). (For
example, a PsychInfo search for ego development yielded 2,897 results, while searches for other characteristic adaptations, such as attachment, yielded many more [17,855].) There are at least three ways
1674
Zinbarg, Uliaszek, & Adler
in which the study of ED can inform the study and practice of psychotherapy.
First, King and her colleagues (e.g., King & Napa, 1998) found
that lay conceptions of ‘‘the good life’’ include both subjective wellbeing as well as leading a life of complex meaning (high ED). They
therefore suggest that clinicians broaden their conception of the desired outcomes of therapy to include an increase in the nuance and
depth of a client’s self-understanding. Ego stage is unlikely to be
related to the client’s trait profile, while their level of happiness might
be predicted by neuroticism and extraversion.
Second, a client’s stage of ED has implications for their treatment.
Dill and Noam (1990) found that individuals at higher stages of ED
tended to request psychodynamic, insight-oriented therapy, whereas
individuals at lower stages of ED tended to request more behavioral
treatments and triage-type interventions that focused on immediate
problem solving. As behavior therapy has become increasingly integrated with cognitive techniques and theory (e.g., Zinbarg, 1990),
however, CBT may have gained some ground in preferences among
those at higher stages of ED since the time that Dill and Noam
collected their data, especially among those aware of the emphasis
on meaning in contemporary CBT. Once in treatment, theory
suggests that individuals at varying stages of ED might also bring
different concerns to therapy. For example, Noam (1998) suggests
that each stage of ED might bring with it certain specific vulnerabilities that could not be predicted from knowing the client’s trait
profile.
Finally, variation in ED is related to the stories clients tell about
their treatment experience, above and beyond that explained by
traits (e.g., Adler & McAdams, 2007, in press). For example, Adler,
Wagner, and McAdams (2007) found that ED was significantly positively correlated with the coherence of individuals’ stories about
their experiences in therapy, even after partialing O. As an increase
in coherence of narratives over the course of treatment may correlate
with outcome (e.g., Baerger & McAdams, 1999; Foa, Molnar, &
Cashman, 1995), therapists might do well to assist their clients at
lower stages of ED to develop more coherent narratives. Thus, ED, a
relatively stable construct in the adult years, may build upon traits’
contribution to the development and maintenance of psychiatric
disorders by influencing their expression in individuals at different
ED stages and may suggest varying treatment strategies.
Personality Traits and Psychotherapy
1675
Narrative identity
There has been increasing theoretical and empirical attention paid to
the relationship between narrative identity and psychotherapy beyond the influence of traits as well, leading some to declare ‘‘narrative as a nontrivial point of convergence for the therapy field’’
(Angus & McLeod, 2004, p. 373; see also Singer, 2005). There is also
evidence that narrative themes relate to psychopathology even after
partialing relevant personality traits. For example, Adler, Kissel,
and McAdams (2006) found that the narrative theme of contamination was strongly related to individuals’ depression and low life
satisfaction, even partialing N. Within the narrative tradition, psychotherapy has been conceived of in two ways: as a process that is
fundamentally concerned with modifying people’s self-narratives
(e.g., White & Epston, 1990) and also as an important source of
personality development that must itself get storied and incorporated into one’s evolving sense of self (e.g., Lieblich, 2004).
The first perspective holds that, regardless of the specific content
of the treatment, therapy is, in essence, about helping clients modify
their self-stories. This viewpoint has led to the development of therapeutic techniques that are explicitly focused on clients’ self-narratives (e.g., White & Epston, 1990). In addition, various components
of clients’ narratives have been operationalized as important process
and outcome indices, independent of traditional symptom-based
measures (e.g., Hayes, Beevers, Feldman, Laurenceau, & Perlman,
2005; Lysaker, Lancaster, & Lysaker, 2003). For example, Lysaker
and colleagues (2003) found that the coherence of the personal
narratives of adults with schizophrenia increased over the course
of treatment. While certain traits might predispose people to craft
certain types of stories about their lives, the themes assessed at the
level of narrative identity have been shown to be correlated with
certain forms of psychopathology, such as depression, after partialing traits like N (Adler et al., 2006).
From the second perspective, the experience of going to therapy is
itself conceived of as an important event that must be incorporated
into the client’s evolving self-story (e.g., Lieblich, 2004). In a classic
work on psychotherapy, Frank (1961) suggested that weaving the
‘‘myth’’ of the therapeutic experience is fundamental to the individual’s continued optimal functioning once treatment has ended
(p. 327). Yet there are significant individual differences in the
1676
Zinbarg, Uliaszek, & Adler
narration of psychotherapy and these differences correlate with variations in mental health (e.g., Adler, Wagner et al., 2007; Baerger &
McAdams, 1999). For example, Adler and McAdams (2007, in
press) found that individuals high in psychological well-being (compared to those low) tended to recall their therapy as the story of a
victorious battle from the past, wherein a personal problem rises to
become (temporarily) a fierce antagonist, only to be defeated once
and for all by a reenergized self (for a related discussion of client
agency, see Combs & Freedman, 2004). In doing CBT for anxiety,
our experience suggests that for many patients it is important to
transform a self-story of being cowardly because of the experience of
intense anxiety to one of being courageous because of action in the
face of anxiety. The thematic content of clients’ narratives and their
evolution over treatment cannot be predicted well from their trait
profiles, yet they serve an important psychological function (e.g.,
Frank, 1961).
CONCLUSION
We have argued that taking personality into account may be useful
for psychotherapists and psychotherapy researchers. Specifically, individual differences in personality traits as well as personality constructs beyond traits such as ego development and narrative identity
appear to have implications for such diverse aspects of psychotherapy as prognosis, treatment-seeking preferences, choice of therapeutic strategies, the focus of therapeutic interventions, and the ways in
which clients regard their treatment and narrate their experiences in
therapy. Clearly, many of the implications we have drawn involve
some degree or other of speculation. It is just as clear to us, however,
that our conjectures are imminently testable. Thus, time and empirical studies will tell which of the hypotheses generated here are valid
or clinically useful and which are not.
Given that the principles of learning theory provide the conceptual foundation for behavior therapy and that much of Eysenck’s
work centered around hypothesized effects of heritable traits in
moderating learning processes and outcomes (e.g., Eysenck, 1967), it
is certainly the case that the perspective adopted here is far more
consistent with the Eysenckian/European school of behavior therapy
than the school that developed in the United States in the 1950s
Personality Traits and Psychotherapy
1677
(Krueger & Piasecki, 2002). A potentially interesting historical note,
however, is that whereas Eysenck in many ways pioneered the modern study of traits (e.g., Eysenck, 1947), the trait-psychopathology
interface (e.g., Eysenck, 1944), behavior therapy (e.g., Eysenck,
1959, 1960a), and the study of the efficacy of psychotherapy (e.g.,
Eysenck, 1952), we are not aware of much research conducted by
Eysenck himself at the trait-psychotherapy interface. In fact,
whereas a PsycINFO search yielded 663 publications authored or
coauthored by Eysenck, including 360 hits using the keyword
personality and another 82 using the keywords psychotherapy and
behavior therapy, we are aware of only three articles or chapters in
which he explicitly discussed the implications of traits for psychotherapy (Eysenck, 1960b, 1969, 1985). Regardless of the ultimate fate
of many of our conjectures, we are convinced that further merging of
these two research streams pioneered by Eysenck will lead to
enhanced understanding and improved practice of psychotherapy.
REFERENCES
Addis, M. E., & Jacobson, N. S. (2000). A closer look at the treatment rationale
and homework compliance in cognitive-behavioral therapy for depression.
Cognitive Therapy and Research, 24, 313–326.
Adler, J. M., Kissel, E., & McAdams, D. P. (2006). Emerging from the CAVE:
Attributional style and the narrative study of identity in midlife adults.
Cognitive Therapy and Research, 30, 39–51.
Adler, J. M., & McAdams, D. P. (2007). The narrative reconstruction of
psychotherapy. Narrative Inquiry, 17, 179–202.
Adler, J. M., & McAdams, D. P. (in press). The narrative reconstruction of
psychotherapy and psychological health. Psychotherapy Research.
Adler, J. M., Wagner, J. W., & McAdams, D. P. (2007). Personality and the coherence of psychotherapy narratives. Journal of Research in Personality, 41,
1179–1198.
Andrews, G., Page, A. C., & Neilson, M. (1993). Sending your teenagers away.
Controlled stress decreases neurotic vulnerability. Archives of General Psychiatry, 50 (7), 585–589.
Angus, L. E., & McLeod, J. (2004). Toward an integrative framework for understanding the role of narrative in the psychotherapy process. In L. E. Angus
& J. McLeod (Eds.), The handbook of narrative and psychotherapy: Practice,
theory, and research (pp. 367–374). Thousand Oaks, CA: Sage.
Baerger, D. R., & McAdams, D. P. (1999). Life story coherence and its relation to
psychological well-being. Narrative Inquiry, 9 (1), 69–96.
Bagby, R. M., Levitan, R. D., Kennedy, S. H., Levitt, A. J., & Joffe, R. T. (1999).
Selective alteration of personality in response to noradrenergic and serotoner-
1678
Zinbarg, Uliaszek, & Adler
gic antidepressant medication in a depressed sample: Evidence of non-specificity. Psychiatry Research, 86, 211–216.
Beck, A. T., Freeman, A., & Davis, D. D. (2004). Cognitive therapy of personality
disorders (2nd ed.). New York: Guilford Press.
Biederman, J., Rosenbaum, J. F., Bolduc-Murphy, E. A., Faraone, S. V., Chaloff,
J., Hirshfeld, D. R., et al. (1993). A three-year follow-up of children with and
without behavioral inhibition. Journal of the American Academy of Child and
Adolescent Psychiatry, 52, 814–821.
Biederman, J., Rosenbaum, J. F., Hirshfeld, D. R., Faraone, S. V., Bolduc, E. A.,
Gersten, M., et al. (1990). Psychiatric correlates of behavioral inhibition in
young children of parents with and without psychiatric disorders. Archives of
General Psychiatry, 47, 21–26.
Blatt, S. J., & Zuroff, D. C. (2005). Empirical evaluation of the assumptions in
identifying evidence based treatments in mental health. Clinical Psychology
Review, 25, 459–486.
Borkovec, T. D., Abel, J. L., & Newman, H. (1995). Effects of psychotherapy on
comorbid conditions in generalized anxiety disorder. Journal of Consulting and
Clinical Psycholgoy, 63, 479–483.
Borkovec, T. D., & Whisman, M. A. (1996). Psychosocial treatment for generalized anxiety disorder. In M. R. Mavissakalian & R. F. Prien (Eds.), Longterm treatments of anxiety disorders (pp. 171–199). Washington, DC: American Psychiatric Association.
Brown, T. A., & Barlow, D. H. (1992). Comorbidity among anxiety disorders:
Implications for treatment and DSM-IV. Journal of Consulting and Clinical
Psychology, 60, 835–844.
Burns, D. D., & Spangler, D. L. (2000). Does psychotherapy homework lead to
improvements in depression in cognitive-behavioral therapy or does improvement lead to increased homework compliance? Journal of Consulting and
Clinical Psychology, 68, 46–56.
Castonguay, L. G., Goldfried, M. R., Wiser, S., Raue, P. J., & Hays, A. M.
(1996). Predicting the effect of cognitive therapy for depression: A study of
unique and common factors. Journal of Consulting and Clinical Psychology, 64,
497–504.
Clark, L. A., Vittengl, J. R., Kraft, D., & Jarrett, R. B. (2003). Separate personality traits from states to predict depression. Journal of Personality Disorders,
17, 152–172.
Clark, L. A., & Watson, D. (1991). Tripartite model of anxiety and depression:
Psychometric evidence and taxonomic implications. Journal of Abnormal
Psychology, 100, 316–336.
Clark, L. A., Watson, D., & Mineka, S. (1994). Temperament, personality, and
the mood and anxiety disorders. Journal of Abnormal Psychology, 103,
103–116.
Cloninger, C. R. (1986). A unified biosocial theory of personality and its role in
the development of anxiety states. Psychiatric Developments, 3, 167–226.
Coid, J., Yang, M., Tyrer, P., Roberts, A., & Ullrich, S. (2006). Prevalence and
correlates of personality disorders in Great Britain. British Journal of Psychiatry, 188, 423–431.
Personality Traits and Psychotherapy
1679
Combs, G., & Freedman, J. (2004). A poststructuralist approach to narrative
work. In L. E. Angus & J. McLeod (Eds.), The handbook of narrative and psychotherapy: Practice, theory, and research (pp. 137–155). Thousand Oaks, CA:
Sage.
Costa, P. T., Bagby, R. M., Herbst, J. H., & McCrae, R. R. (2005). Personality
self-reports are reliable and valid during acute depressive episodes. Journal of
Affective Disorders, 89, 45–55.
Costa, P. T., & McCrae, R. R. (1997). Normal personality assessment in clinical
practice: The NEO Personality Inventory. Psychological Assessment, 4 (1),
5–13.
Cronbach, L. J., & Gleser, G. C. (1957). Psychological tests and personnel decisions. Urbana: University of Illinois.
De Fruyt, F., Van Leeuwen, K., Bagby, R. M., Rolland, J., & Rouillon, F. (2006).
Assessing and interpreting personality change and continuity in patients
treated for major depression. Psychological Assessment, 18 (1), 71–80.
Depue, R. A., & Iacono, W. G. (1989). Neurobehavioral aspects of affective
disorders. Annual Review of Psychology, 40, 457–492.
Digman, J. M. (1997). Higher-order factors of the big five. Journal of Personality
and Social and Psychology, 73 (6), 1246–1256.
Dill, D. L., & Noam, G. G. (1990). Ego development and treatment requests.
Psychiatry, 53, 85–91.
Du, L., Bakish, D., Ravindran, A. V., & Hrdina, P. D. (2002). Does fluoxetine
influence major depression by moderating the five-factor personality traits?
Journal of Affective Disorders, 71, 235–241.
Durbin, C. E., Klein, D. N., Hayden, E. P., Buckley, M. E., & Moerk, K. C.
(2005). Temperamental Emotionality in Preschoolers and Parental Mood
Disorders. Journal of Abnormal Psychology, 114, 28–37.
Ehlers, A. (1995). A 1-year prospective study of panic attacks: Clinical course and
factors associated with maintenance. Journal of Abnormal Psychology, 104,
164–172.
Eysenck, H. J. (1944). Types of personality: A factorial study of seven hundred
neurotics. Journal of Mental Science, 90, 851–861.
Eysenck, H. J. (1947). Dimensions of personality. London: Routledge & Kegan
Paul.
Eysenck, H. J. (1952). The effects of psychotherapy: An evaluation. Journal of
Consulting Psychology, 16, 319–324.
Eysenck, H. J. (1959). Learning theory and behaviour therapy. Journal of Mental
Science, 105, 61–75.
Eysenck, H. J. (1960a). Behavior therapy and the neuroses. Oxford: Pergamon
Press.
Eysenck, H. J. (1960b). Levels of personality, constitutional factors, and social
influences: An experimental approach. International Journal of Social Psychiatry, 6, 12–24.
Eysenck, H. J. (1967). The biological basis of personality. Springfield, IL: Charles
C. Thomas.
Eysenck, H. J. (1969). Relapse and symptom substitution after different types of
psychotherapy. Behaviour Research & Therapy, 7, 283–287.
1680
Zinbarg, Uliaszek, & Adler
Eysenck, H. J. (1985). Incubation theory of fear/anxiety. In S. Reiss & R. R.
Bootzin (Eds.), Theoretical issues in behavior therapy (pp. 83–105). New York:
Academic Press.
Eysenck, H. J. (1992). Four ways five factors are not basic. Personality and
Individual Differences, 13, 667–673.
Ferguson, D. M., Horwood, L. J., & Boden, J. M. (2006). Structure of
internalizing symptoms in early adulthood. British Journal of Psychiatry,
189, 540–546.
Foa, E. B., Molnar, C., & Cashman, L. (1995). Change in rape narratives during
exposure therapy for posttraumatic stress disorder. Journal of Traumatic
Stress, 8 (4), 675–690.
Forsyth, J. P., Palav, A., & Duff, K. (1999). The absence of relation
between anxiety sensitivity and fear conditioning using 20% versus 13%
CO2-enriched air as unconditioned stimuli. Behaviour Research and Therapy,
37, 143–153.
Fowles, D. C. (1993). Biological variables in psychopathology: a psychobiological
perspective. In P. B. Sutker & H. E. Adams (Eds.), Comprehensive handbook of
psychopathology (pp. 57–82). New York: Plenum Press.
Fraley, R. C., & Roberts, B. W. (2005). Patterns of continuity: A dynamic
model for conceptualizing the stability of individual differences in
psychological constructs across the life course. Psychological Review, 112,
60–74.
Frank, J. D. (1961). Persuasion and healing: A comprehensive study of psychotherapy. Baltimore: Johns Hopkins University Press.
Gershuny, B. S., & Sher, K. J. (1998). The relation between personality and
anxiety: Findings from a 3-year prospective study. Journal of Abnormal
Psychology, 107, 252–262.
Goldberg, L.R (1993). The structure of phenotypic personality traits. American
Psychologist, 48 (1), 26–34.
Gottesman, I. I. (1963). Genetic aspects of intelligent behavior. In N. Ellis (Ed.),
Handbook of mental deficiency: Psychological theory and research (pp.
253–296). New York: McGraw-Hill.
Gray, J. A., & McNaughton, N. (2000). The neuropsychology of anxiety. Oxford:
Oxford University Press.
Gregory, A. M., Caspi, A., Moffitt, T. E., Koenen, K., Eley, T. C., & Poulton, R.
(2007). Juvenile mental health histories of adults with anxiety disorders.
American Journal of Psychiatry, 164, 301–308.
Gurtman, M. B. (1996). Interpersonal problems and the psychotherapy context:
The construct validity of the inventory of interpersonal problems. Psychological Assessment, 8 (3), 241–255.
Hampson, S. E., & Goldberg, L. R. (2006). A first large cohort study of personality trait stability over the 40 years between elementary school and midlife.
Journal of Personality and Social Psychology, 91, 763–779.
Hampson, S. E., John, O. P., & Goldberg, L. R. (1986). Category breadth
and hierarchical structure in personality: Studies of asymmetries in judgments
of trait applications. Journal of Personality and Social Psychology, 51 (1),
37–54.
Personality Traits and Psychotherapy
1681
Harkness, A. R., & Lilienfeld, S. O. (1997). Individual differences science for
treatment planning: Personality traits. Psychological Assessment, 9 (4),
349–360.
Hayes, A. M., Beevers, C., Feldman, G., Laurenceau, J-P., & Perlman, C. A.
(2005). Avoidance and emotional processing as predictors of symptom change
and positive growth in an integrative therapy for depression. International
Journal of Behavioral Medicine, 12, 111–122.
Hayward, C., Killen, J. D., Kraemer, H. C., & Taylor, C. B. (1998). Linking selfreported childhood behavioral inhibition to adolescent social phobia. Journal
of the American Academy of Child & Adolescent Psychiatry, 37, 1308–1316.
Hayward, C., Killen, J. D., Kraemer, H. C., & Taylor, C. B. (2000). Predictors
of panic attacks in adolescence. Journal of the American Academy of Child &
Adolescent Psychiatry, 39, 207–214.
Hettema, J. M., Neale, M. C., & Kendler, K. S. (2001). A review and meta-analysis of genetic epidemiology of anxiety disorders. American Journal of Psychiatry, 158 (10), 1568–1578.
Hettema, J. M., Neale, M. C., Myers, J. M., Prescott, C. A., & Kendler, K. S.
(2006). A population-based twin study of the relationship between neuroticism
and internalizing disorders. American Journal of Psychiatry, 163, 857–864.
Hettema, J. M., Prescott, C. A., Myers, J. M., Neale, M. C., & Kendler, K. S.
(2005). The structure of genetic and environmental risk factors for anxiety
disorders in men and women. Archives of General Psychiatry, 62, 182–189.
Hirschfeld, D. R., Rosenbaum, J. F., Biederman, J., Bolduc, E. A., Faraone, S. V.,
Snidman, N., et al. (1992). Stable behavioral inhibition and its association with
anxiety disorders. Journal of the American Academy of Child and Adolescent
Psychiatry, 31, 103–111.
Hirschfeld, R. M. A., Klerman, G. L., Clayton, P. J., & Keller, M. B. (1983).
Personality and depression: Empirical findings. Archives of General Psychiatry,
40, 993–998.
Hirschfeld, R. M. A., Klerman, G. L., Lavori, P., Keller, M. B., Griffith, P., &
Coryell, W. (1989). Premorbid personality assessments of first onset of major
depression. Archives of General Psychiatry, 46, 345–350.
Holahan, C. J., & Moos, R. H. (1991). Life stressors, personal and social
resources, and depression: A 4-year structural model. Journal of Abnormal
Psychology, 100, 31–38.
Jacobson, N. S., Dobson, K. S., Truax, P. A., Addis, M. E., Koerner, K., Gollan,
J. K., et al. (1996). A component analysis of cognitive-behavioral treatment for
depression. Journal of Consulting and Clinical Psychology, 64, 295–304.
Jang, K. L., McCrae, R. R., Angleitner, A., Riemann, R., & Livesley, W. J.
(1998). Heritability of facet-level traits in a cross-cultural twin sample: Support
for a hierarchical model of personality. Journal of Personality and Social
Psychology, 74 (6), 1556–1565.
John, O., Hampson, S. E., & Goldberg, L. R. (1991). The basic level in personality-trait hierarchies: Studies of trait use and accessibility in different contexts.
Journal of Personality and Social Psychology, 60 (3), 348–361.
Jorm, A. F., Christensen, H., Henderson, A. S., Jacomb, P. A., Korten, A. E., &
Rodgers, B. (2000). Predicting anxiety and depression from personality: Is
1682
Zinbarg, Uliaszek, & Adler
there a synergistic effect of neuroticism and extraversion? Journal of Abnormal
Psychology, 109, 145–149.
Kazantis, N., Deane, F. P., & Ronan, K. R. (2000). Homework assignments
in cognitive and behavioral therapy: A meta-analysis. Clinical Psychology:
Science and Practice, 7, 189–202.
Keller, M. C., Coventry, W. L., Heath, A. C., & Martin, N. G. (2005). Widespread evidence for non-additive genetic variation in Cloninger’s and
Eysenck’s personality dimensions using a twin plus sibling design. Behavior
Genetics, 35 (6), 707–721.
Kendler, K. S., Gatz, M., Gardner, C. O., & Pedersen, N. L. (2006). Personality
and major depression: A Swedish longitudinal, population-based twin study.
Archives of General Psychiatry, 63, 1113–1120.
Kendler, K. S., Kuhn, J., & Prescott, C. A. (2004). The interrelationship of
neuroticism, sex, and stressful life events in the prediction of episodes of Major
Depression. American Journal of Psychiatry, 161, 631–636.
Kendler, K. S., Neale, M. C., Kessler, R. C., Heath, A. C., & Eaves, L. J. (1993).
A longitudinal twin study of personality and major depression in women.
Archives of General Psychiatry, 50, 853–862.
Kendler, K. S., Prescott, C. A., Myers, J., & Neale, M. C. (2003). The structure of
genetic and environmental risk factors for common psychiatric and substance
use disorders in men and women. Archives of General Psychiatry, 60, 929–937.
King, L. A., & Napa, C. K. (1998). What makes a life good? Journal of Personality
and Social Psychology, 75 (1), 156–165.
Klein, D. N., Schwartz, J. E., Santiago, N. J., Vivian, D., Vocisano, C., &
Castonguay, L. G. (2003). Therapeutic alliance in depression treatment: Controlling for prior change and patient characteristics. Jounral of Consulting and
Clinical Psychology, 71, 997–1006.
Krueger, R. F. (1999). The structure of common mental disorders. Archives of
General Psychiatry, 56, 921–926.
Krueger, R. F. (2005). Continuity of Axis I and Axis II: Toward a unified model
of personality, personality disorders, and clinical disorders. Journal of Personality Disorders, 19 (3), 233–261.
Krueger, R. F., Caspi, A., Moffitt, T. E., & Silva, P. A. (1998). The structure
and stability of common mental disorders (DSM-III-R): A longitudinal-epidemiological study. Journal of Abnormal Psychology, 107, 216–227.
Krueger, R. F., Caspi, A., Moffitt, T. E., Silva, P. A., & McGee, R. (1996). Personality traits are differentially linked to mental disorders: A multitrait-multidiagnosis study of an adolescent birth cohort. Journal of Abnormal
Psychology, 105, 299–312.
Krueger, R. F., Chentsova-Dutton, Y. E., Markon, K. E., Goldberg, D., &
Ormel, J. (2003). A cross-cultural study of the structure of comorbidity among
common psychopathological syndromes in the general health care setting.
Journal of Abnormal Psychology, 112, 437–447.
Krueger, R. F., & Johnson, W. (2007). Behavioral genetics and personality: A new
look at the integration of nature and nurture. L. A., Pervin, O. P. John, &
R. W. Robins (Eds.), Handbook of personality: Theory and research (3rd ed.).
New York: Guilford.
Personality Traits and Psychotherapy
1683
Krueger, R. F., & Piasecki, T. M. (2002). Toward a dimensional and psychometrically informed approach to conceptualizing psychopathology. Behaviour
Research and Therapy, 4, 485–500.
Krueger, R. F., South, S., Johnson, W., & Iacono, W. (in press). The
heritability of personality is not always 50%: Gene-environment
interactions and correlations between personality and parenting. Journal of
Personality.
Krupnick, J. L., Sotsky, S. M., Elkin, I., Simmens, S., Moyer, J., Watkins, J., et al.
(1996). The role of the therapeutic alliance in psychotherapy and pharmacotherapy outcome: Findings in the National Institute of Mental Health Treatment of Depression Collaborative Research Program. Journal of
Consulting and Clinical Psychology, 64, 532–539.
Lenzenweger, M. F. (2006). The Longitudinal Study of Personality Disorders:
History, design, considerations, and initial findings. Journal of Personality
Disorders, 20 (6), 645–670.
Levenson, M. R., Aldwin, C. M., Bosse, R., & Spiro, A. (1988). Emotionality and
mental health: Longitudinal findings from the normative aging study. Journal
of Abnormal Psychology, 97, 94–96.
Levinson, D. F. (2005). The genetics of depression: A review. Biological Psychiatry, 60, 84–92.
Li, W., & Zinbarg, R. (2007). Anxiety sensitivity and panic: A one-year longitudinal
study. Behavior Modification, 31, 145–161. DOI: 10.1177/0145445506296969.
Lieblich, A. (2004). The place of psychotherapy in the life stories of women in
households without men. In A. Lieblich, D. P. McAdams, & R. Josselson
(Eds.), Healing plots: The narrative basis of psychotherapy (pp. 171–188).
Washington, DC: American Psychological Association.
Lilienfeld, S. O., Turner, S. M., & Jacob, R. G. (1993). Anxiety sensitivity: An
examination of theoretical and methodological issues. Advances in Behaviour
Research and Therapy, 15, 147–183.
Linehan, M. M., Armstrong, H. E., Suarez, A., Allmon, D., & Heard, H. L.
(1991). Cognitive-behavioral treatment of chronically parasuicidal borderline
patients. Archives of General Psychiatry, 48, 1060–1064.
Link, B., & Dohrenwend, B. P. (1980). Formulation of hypotheses about the true
prevalence of demoralization in the United States. In B. P. Dohrenwend, B. S.
Dohrenwend, M. Gould, B. Link, R. Neugebauer, & R. Wunsch-Hitzig (Eds.),
Mental illness in the United States (pp. 114–132). New York: Praeger Publications.
Livesley, J. (2007). Introduction to special feature on borderline personality
disorder: Part 1. Journal of Personality Disorders, 21, 455–456.
Livesley, W. J. (2004). Introduction to the special feature on recent progress
in the treatment of personality disorder. Journal of Personality Disorders, 18,
1–2.
Loeb, K. L., Wilson, T. G., Labouvie, E., Pratt, E. M., Hayaki, J., & Walsh, B. T.
(2005). Therapeutic alliance and treatment adherence in two interventions for
bulimia nervosa: A study of process and outcome. Journal of Consulting and
Clinical Psychology, 73, 1097–1107.
1684
Zinbarg, Uliaszek, & Adler
Loehlin, J. C., Neiderhiser, J. M., & Reiss, D. (2003). The behavior genetics of
personality and the NEAD study. Journal of Research in Personality, 37, 373–
387.
Loevinger, J. (1976). Edo development: Conceptions and theories. San Francisco:
Jossey Bass.
Luborsky, L., McLellan, A. T., Woody, G. E., O’Brien, C. P., & Auerbach, A.
(1985). Therapist success and its determinants. Archives of General Psychiatry,
42, 602–611.
Lysaker, P. H., Lancaster, R. S., & Lysaker, J. T. (2003). Narrative transformation as an outcome in the psychotherapy of schizophrenia. Psychology and
Psychotherapy: Theory, Research and Practice, 76(3), 285–299.
MacKintosh, M., Gatz, M. M., Wetherell, J. L., & Pedersen, N. L. (2006). A twin
study of lifetime generalized anxiety disorder (GAD) in older adults: Genetic
and environmental influences shared by neuroticism and GAD. Twin Research
and Human Genetics, 9(1), 30–37.
Markon, K. E., Krueger, R. F., & Watson, D. (2005). Delineating the structure of
normal and abnormal personality: An integrative hierarchical approach.
Journal of Personality and Social Psychology, 88, 139–157.
Martell, C. R., Addis, M. E., & Jacobson, N. S. (2001). Depression in context:
Strategies for guided action. New York: W. W. Norton.
Mathews, A., Mogg, K., Kentish, J., & Eysenck, M. (1995). Effect of psychological treatment on cognitive bias in generalized anxiety disorder. Behaviour
Research and Therapy, 33, 293–303.
McAdams, D. P. (1995). What do we know when we know a person? Journal
of Personality, 63, 365–396.
McAdams, D. P. (2001). The psychology of life stories. Review of General
Psychology, 5 (2), 100–122.
McAdams, D. P., & Pals, J. L. (2006). A new big five: Fundamental principles
for an integrative science of personality. American Psychologist, 61(3),
204–217.
McCrae, R. R. (1991). The five-factor model and its assessment in clinical settings.
Journal of Personality Assessment, 57(3), 399–414.
McCrae, R. R., & Costa, P. T. (1996). Toward a new generation of personality
theories: Theoretical contexts for the five-factor model. Wiggins, Jerry S. (Ed.).
The five-factor model of personality: Theoretical perspectives (pp. 51–87). New
York: Guilford Press.
McCrae, R. R., Jang, K. L., Livesley, W. J., Riemann, R., & Angleitner, A.
(2001). Sources of structure: Genetic, environmental, and artifactual influences
on the covariation of personality traits. Journal of Personality, 64(4), 511–535.
McGue, M., Bacon, S., & Lykken, D. T. (1993). Personality stability and change
in early adulthood: A behavioral genetic analysis. Developmental Psychology,
29(1), 96–109.
McGue, M., Bouchard, T., Iacono, W., & Lykken, D.T. (1993). Behavioral genetics of cognitive ability: A life-span perspective. In R. Plomin & G. E. McClearn (Eds.), Nature, nurture, and psychology (pp. 59–76). Washington, DC:
American Psychological Association.
Personality Traits and Psychotherapy
1685
McNally, R. J. (1996). Anxiety sensitivity is distinguishable from trait anxiety. In
R. M. Rapee (Ed.), Current controversies in the anxiety disorders (pp. 214–227).
New York: Guilford Press.
Merzenich, M. (1998). Long-term change of mind. Science, 282, 1062–1063.
Miller, J. D., Lynam, D. R., Widiger, T. A., & Leukefeld, C. (2001). Personality
disorders as extreme variants of common personality dimensions: Can the
Five-Factor Model adequately represent psychopathy? Journal of Personality,
69, 253–276.
Miller, T. R. (1991). The psychotherapeutic utility of the five-factor model of personality: A clinician’s experience. Journal of Personality Assessment, 57, 415–433.
Muten, E. (1991). Self-reports, spouse ratings, and psychophysiological assessment in a behavioral medicine program: An application of the five-factor
model. Journal of Personality Assessment, 57(3), 449–464.
Muthen, B. (1984). A general structural equation model with dichotomous, ordered categorical, and continuous latent variable indicators. Psychometrika,
49, 115–132.
Noam, G. G. (1998). Solving the ego development-mental health riddle. In P. M.
Westenberg, A. Blasi, & L. D. Cohn (Eds.), Personality development: Theoretical, empirical, and clinical investigations of Loevinger’s conception of
ego development (pp. 271–295). Mahwah, NJ: Lawrence Erlbaum Associates.
O’Connor, B. P. (2002). The search for dimensional structure differences between
normality and abnormality: A statistical review of published data on personality and psychopathology. Journal of Personality and Social Psychology, 83
(4), 962–982.
O’Connor, B. P., & Dyce, J. A. (2001). Rigid and extreme: A geometric representation of personality disorders in five-factor model space. Journal of
Personality and Social Psychology, 81(6), 1119–1130.
Ogrodniczuk, J. S., Piper, W. E., Joyce, A. S., McCallum, M., & Rosie, J. S.
(2003). NEO-Five factor personality traits as predictors of response to two
forms of group psychotherapy. International Journal of Group Psychotherapy,
53(4), 417–442.
Ormel, J., Oldehinkel, A. J., & Vollebergh, W. (2004). Vulnerability before, during, and after a major depressive episode: A 3-wave population-based study.
Archives of General Psychiatry, 61, 990–996.
Plomin, R., & Spinath, F. M. (2004). Intelligence: Genetics, genes and genomics.
Journal of Personality and Social Psychology, 86, 112–119.
Rapee, R. M., & Medoro, L. (1994). Fear of physical sensations and trait anxiety
as mediators of the response to hyperventilation in nonclinical subjects.
Journal of Abnormal Psychology, 103, 693–699.
Reiss, S. (1980). Pavlovian conditioning and human fear: An expectancy model.
Behavior Therapy, 11, 380–396.
Roberts, B. W., Caspi, A., & Moffitt, T. E. (2003). Work experiences and personality development in young adulthood. Journal of Personality and Social
Psychology, 84(3), 582–593.
Roberts, B. W., & DelVecchio, W. F. (2000). The rank-order consistency of personality traits from childhood to old age: A quantitative review of longitudinal
studies. Psychological Bulletin, 126, 3–25.
1686
Zinbarg, Uliaszek, & Adler
Santor, D. A., Bagby, R. M., & Joffe, R. T. (1997). Evaluating stability
and change in personality and depression. Journal of Personality and Social
Psychology, 73(6), 1354–1362.
Saudino, K. J., & Plomin, R. (1996). Personality and behavioral genetics: Where
have we been and where are we going? Journal of Research in Personality, 30,
335–347.
Saudino, K. J., Plomin, R., & DeFries, J. C. (1996). Tester-rated temperament at
14, 20 and 24 months: Environmental change and genetic continuity. British
Journal of Developmental Psychology, 14 (2), 129–144.
Schwartz, C. E., Snidman, N., & Kagan, J. (1999). Adolescent social anxiety as an
outcome of inhibited temperament in childhood. Journal of the American
Academy of Child & Adolescent Psychiatry, 38, 1008–1015.
Schmidt, N. B., Lerew, D. R., & Jackson, R. J. (1999). Prospective evaluation of
anxiety sensitivity in the pathogenesis of panic: Replication and extension.
Journal of Abnormal Psychology, 108, 532–537.
Shahar, G., Blatt, S. J., Zuroff, D. C., Krupnick, J. L., & Sotsky, S. M. (2004).
Perfectionism impedes social relations and response to brief treatment for
depression. Journal of Social and Clinical Psychology, 23, 140–154.
Singer, J. A. (2004). Narrative identity and meaning making across the adult
lifespan: An introduction. Journal of Personality, 72(3), 437–460.
Singer, J. A. (2005). Personality and psychotherapy: Treating the whole person.
New York: Guilford Press.
Sturges, L. V., Goetsch, V., Ridley, J., & Whittal, M. (1998). Anxiety
sensitivity and response to hyperventilation challenge: Physiologic arousal, interoceptive acuity, and subjective distress. Journal of Anxiety Disorders, 12,
103–115.
Sullivan, P. F., Neale, M. C., & Kendler, K. S. (2000). Genetic epidemiology of
major depression: Review and meta-analysis. American Journal of Psychiatry,
157, 1552–1562.
Takane, Y., & de Leeuw, J. (1987). On the relationship between item
response theory and factor analysis of discretized variables. Psychometrika,
52, 393–408.
Tang, T. Z., DeRubeis, R. J., Hollon, S. D., Shelton, R., & Schalet, B. (in preparation). Personality changes during SSRI-treatment and the repair of key
causes of depression.
Tellegen, A. (1985). Structures of mood and personality and their relevance
to assessing anxiety, with an emphasis on self-report. In A. H. Tuma &
J. D. Maser (Eds.), Anxiety and the anxiety disorders (pp. 681–706). Hillsdale,
NJ: Lawrence Erlbaum Associates, Inc.
Turner, S. M., Beidel, D. C., & Wolff, P. L. (1996). Is behavioral inhibition related
to the anxiety disorders? Clinical Psychology Review, 16, 157–172.
Vollebergh, W. A. M., Iedema, J., Bijl, R. V., de Graff, R., Smit, F., & Ormel, J.
(2001). The structure and stability of common mental disorders: The NEMESIS Study. Archives of General Psychiatry, 58, 597–603.
Watson, D., & Humrichouse, J. (2006). Personality development in emerging
adulthood: Integrating evidence from self-ratings and spouse ratings. Journal
of Personality and Social Psychology, 91, 959–974.
Personality Traits and Psychotherapy
1687
Watson, D., Clark, L. A., & Chmielewski, M. (2008). Structures of personality
and their relevance to psychopathology: II. Further articulation of a comprehensive unified trait structure. Journal of Personality, 76(6), 1545–1585.
Weissman, A. N., & Beck, A. T. (1978, August–September). Development and
validation of the dysfunctional attitudes scale: A preliminary investigation. Paper
presented at the 86th annual convention of the American Psychological Association, Toronto, Canada.
Westen, D., Gabbard, G. O., & Blagov, P. (2006). Back to the future: Personality
structure as a context for psychopathology. In R. F. Krueger & J. L. Tackett
(Eds.), Personality and psychopathology (pp. 335–384). New York: Guilford
Press.
Westenberg, P. M., & Block, J. (1993). Ego development and individual differences
in personality. Journal of Personality and Social Psychology, 65, 792–800.
White, M., & Epston, D. (1990). Narrative means to therapeutic ends. New York:
Norton.
Widiger, T. A. (2003). Personality disorder and Axis I psychopathology: The
problematic boundary of Axis I and Axis II. Journal of Personality Disorders,
17(2), 90–108.
Widiger, T. A., & Trull, T. J. (1992). Personality and psychopathology: An
application of the five-factor model. Journal of Personality, 60(2), 363–393.
Zinbarg, R. (1990). Animal research and behavior therapy: Part I: Behavior
therapy is not what you think it is. The Behavior Therapist, 13, 171–175.
Zinbarg, R. (1998). Concordance and synchrony in measures of anxiety and panic
reconsidered: A hierarchical model of anxiety and panic. Behavior Therapy, 29,
301–323.
Zinbarg, R., & Barlow, D. H. (1996). The structure of anxiety and the DSM-III-R
anxiety disorders: A hierarchical model. Journal of Abnormal Psychology, 105,
181–193.
Zinbarg, R., Barlow, D. H., & Brown, T. (1997). The hierarchical structure and
general factor saturation of the Anxiety Sensitivity Index: Evidence and
implications. Psychological Assessment, 9, 277–284.
Zinbarg, R., Brown, T. A., Barlow, D. H., & Rapee, R. M. (2001). Anxiety
sensitivity, panic and depressed mood: A re-analysis teasing apart the contributions of the two levels in the hierarchical structure of the anxiety sensitivity
index. Journal of Abnormal Psychology, 110, 372–378.
Zinbarg, R., Lee, J. E., & Yoon, L. (2007). Dyadic predictors of outcome in a
cognitive-behavioral program for patients with generalized anxiety disorder in
committed relationships: A ‘‘spoonful of sugar’’ and a dose of non-hostile
criticism may help. Behaviour Research and Therapy, 45, 699–713.
Zinbarg, R., & Yoon, L. (2008). Reinforcement sensitivity theory and clinical disorders: Anxiety and depression. In P. J. Corr (Ed.), The reinforcement sensitivity
theory of personality (pp. 360–397). Cambridge: Cambridge University Press.
Zuroff, D. C., Blatt, S. J., Sotsky, S. M., Krupnick, J. L., Martin, D. J., Sanislow,
C. A., et al. (2000). Relation of therapeutic alliance and perfectionism to outcome in brief outpatient treatment of depression. Journal of Consulting and
Clinical Psychology, 68, 114–124.
1688