Personalidad y Depresion

8/2/2019 Personalidad y Depresion

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Personality and Depression:Explanatory Models andReview of the Evidence

Daniel N. Klein, Roman Kotov, and Sara J. Buffe

Departments of Psychology and Psychiatry, State University of New York at Stony BStony Brook, New York 11794-2500; email: [email protected]

Annu. Rev. Clin. Psychol. 2011. 7:26995

First published online as a Review in Advance on

December 6, 2010

The Annual Review of Clinical Psychology is onlineat clinpsy.annualreviews.org

This articles doi:10.1146/annurev-clinpsy-032210-104540

Copyright c 2011 by Annual Reviews.All rights reserved

1548-5943/11/0427-0269$20.00

Keywords

traits, temperament, mood disorders, neuroticism, extraversion

Abstract

Understanding the association between personality and depressioimplications for elucidating etiology and comorbidity, identifyin

risk individuals, andtailoring treatment. We discuss seven major mthat have been proposed to explain the relation between personality

depression, and we review key methodological issues, including sdesign, the heterogeneity of mood disorders, and the assessment of

sonality. We then selectively review the extensive empirical literaon the role of personality traits in depression in adults and child

Current evidence suggests that depression is linked to traits su

neuroticism/negative emotionality, extraversion/positive emotionand conscientiousness. Moreover, personality characteristics appecontribute to the onset and course of depression through a varie

pathways. Implications for prevention and prediction of treatmen

sponse are discussed, as well as specific considerations to guide furesearch on the relation between personality and depression.

269

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Temperament:generally used todescribe personality inchildhood; largelyinterchangeable withthe term personality

Neuroticism:a tendency to copepoorly with stress andto experience feelingsof sadness, anxiety, andanger

Contents

INTRODUCTION . . . . . . . . . . . . . . . . . . 270THE CONSTRUCT OF

PERSONALITY . . . . . . . . . . . . . . . . . . 270MODELS OF PERSONALITY

AND DEPRESSION . . . . . . . . . . . . . . 271

Classical Models ofPersonality-DepressionRelations . . . . . . . . . . . . . . . . . . . . . . . 271

Dynamic Models ofPersonality-Depression

Relations . . . . . . . . . . . . . . . . . . . . . . . 274METHODOLOGICAL ISSUES . . . . . 275

Study Design . . . . . . . . . . . . . . . . . . . . . . 275

Heterogeneity of DepressiveD i s o r d e r s . . . . . . . . . . . . . . . . . . . . . . . 2 7 6

Assessment . . . . . . . . . . . . . . . . . . . . . . . . 276

AFFECTIVE TEMPERAMENTS . . . . 277PERSONALITY TRAIT

DIMENSIONS . . . . . . . . . . . . . . . . . . . 279

The Five-Factor Model . . . . . . . . . . . . 279Psychobiological Models . . . . . . . . . . . 283

Clinical Traits . . . . . . . . . . . . . . . . . . . . . 284CHILD TEMPERAMENT . . . . . . . . . . 285

CLINICAL IMPLICATIONS. . . . . . . . 286

Prevention . . . . . . . . . . . . . . . . . . . . . . . . 286Treatment Response . . . . . . . . . . . . . . . 286

CONCLUSIONS AND FUTURE

DIRECTIONS . . . . . . . . . . . . . . . . . . . . 287

INTRODUCTION

The hypothesis that depression is linked to per-sonality can be traced to antiquity, when Hip-

pocrates, and laterGalen, argued thatparticularhumors were responsible for specific per-

sonality types and forms of psychopathology.In this article, we discuss the major conceptual

models that have been proposed to explain theassociationbetweenpersonality and depression,

comment on some important methodological

issues, and selectively review the empiricalliterature. Due to space limitations, we limit

our review to nonbipolar forms of depression.This literature has developed along several

distinct lines: (a) early clinical psychiatrists

descriptions of affective temperamen

(b) research on the structure and neurobioloof personality; (c) psychoanalytic and cognitiv

behavioral theory and observations; a(d) developmental psychologists work

temperament. In recent years, there has be

substantial convergence between these lin

of work, and it is increasingly possible to viethem within a single integrative frameworUnderstanding the associations between pe

sonality and depression has a number of potetially important implications for research an

practice. First, personality traits associated wiemotional experience, expression, and regul

tion may be intermediate phenotypes that prvide more tractable targets for genetic and ne

robiological research than depressive diagnos

(Canli 2008). Second, personality may be usefin identifying more homogeneous subgrou

of depressive disorders that differ in develomental trajectories and etiological influenc

(e.g., Beck 1983). Third, tracing the pathwabetween personality and depressive disorde

can help elucidate more proximal processinvolved in the development of mood disorde

(Compas et al. 2004, Klein et al. 2008a, Lah2009). Fourth, personality may be useful in ta

loring treatment (Zinbarg et al. 2008) and prdicting treatment response (Quilty et al. 2008

Fifth, temperament/personality may provi

a means to identify at-risk individuals wcould benefit from prevention and ear

intervention efforts (Kovacs & Lopez-Dur2010). Finally, there is substantial comorbidi

between depressive disorders and other formof psychopathology. Some personality trai

such as neuroticism, are associated with mutiple psychiatric conditions. Thus, personali

could help explain patterns of comorbidand point toward more etiologically releva

classification systems (Brown & Barlow 200Kotov et al. 2007, Watson 2009).

THE CONSTRUCT OFPERSONALITY

Before addressing the relation between pe

sonality and depression, several conceptu

270 Klein Kotov Bufferd


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issues regarding the construct of personality

should be considered. First, personality hastraditionally been conceptualized as having

two components: temperament, which refersto biologically based, early-emerging, stable

individual differences in emotion and its regu-

lation, and character, which refers to individual

differences due to socialization. However,the distinctions between these constructs arequestionable, as a large body of evidence has

accumulated indicating that personality traitshave all the characteristics of temperament, in-

cluding strong genetic and biological bases andsubstantial stability over the lifespan (Krueger

& Johnson 2008, Watson et al. 2006). Hence,the terms personality and temperament

are now often used interchangeably (Caspi

& Shiner 2006, Clark & Watson 1999). Asmost research on personality in childhood

has been conducted under the temperamentrubric, in this review we refer to this work

using the term temperament and reserve theterm personality for discussing the literature

on adolescents and adults. However, this isintended to reflect traditional usage rather

than a conceptually meaningful distinction.Second, a variety of personality classifica-

tions have been proposed over the past century,but in the 1980s they were integrated in a

consensus taxonomy, the Five-Factor Model

(FFM). The FFM recognized that personalityis ordered hierarchically from a large number

of specific traits to five general characteristics(Digman 1994, Goldberg 1993, Markon et al.

2005). These Big Five traits are neuroticism,extraversion, conscientiousness, agreeableness,

and openness to experience. Importantly,the FFM can be further reduced to three

dimensions of negative emotionality, positiveemotionality, and disinhibition versus con-

straintthatformthenextlevelofthepersonalityhierarchy (Clark & Watson 1999, Markon

et al. 2005). This Big Three model is used in

studies of temperament as well as personality,although disinhibition is often labeled as

effortful control in the child literature (Caspi &Shiner 2006, Rothbart & Bates 2006). The Big

Five and Big Three schemes are closely related,

Five-Factor M(FFM): hierarcpersonality taxowith five generaat its apex:neuroticism,

extraversion,conscientiousneagreeableness, aopenness to exp

Extraversion:tendency to engenvironment anpeople with vigoenthusiasm

Conscientioustendency to apptasks in a planfu

deliberate mannto be reliable anself-disciplined

N/NE: neurotinegative emotio

E/PE: extraverpositive emotion

with neuroticism being essentially identical to

negative emotionality and extraversion cor-responding to positive emotionality (Clark &

Watson 1999, Markon et al. 2005); we refer tothese two dimensions as neuroticism/negative

emotionality (N/NE) and extraversion/positive

emotionality (E/PE), respectively. Disinhi-

bition does not have an exact counterpart inthe FFM but instead reflects a combination oflow conscientiousness and low agreeableness.

Finally, openness to experience is outside theterritory covered by the Big Three.

Third, there is increasing recognitionthat temperament and personality are not a

fixed, static set of characteristics, but ratherare dynamic constructs that develop over the

lifespan and change in response to maturation

and life circumstances (Fraley & Roberts 2005,Rothbart & Bates 2006). For example, although

the rank-order stability of most personalitytraits is in the moderate range, it increases

over the course of development (Roberts &DelVecchio 2000). In addition, mean levels

of conscientiousness and some facets of E/PEincrease, and levels of N/NE decrease, over

time, particularly in young adulthood (Robertset al. 2006). A number of processes contribute

to stability and change of personality. For ex-ample, genes are a major influence on stability

(Krueger & Johnson 2008, Kandler et al. 2010).

In addition,people often select, create, andcon-strue environments in ways that reinforce and

maintain their initial trait dispositions (Caspi &Shiner 2006). However, life stressors and major

shifts in social roles and relationships can con-tribute to personality change (Fraley & Roberts

2005, Kandler et al. 2010). We consider theimplications of these processes for the relation

between personality and depression below.

MODELS OF PERSONALITYAND DEPRESSION

Classical Models ofPersonality-Depression Relations

A variety of models of the relation between

personality and mood disorders have been

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Table 1 Summary of key predictions of the classic models

Model Predictions about a target trait and its relation to depression

Common cause Shared etiology accounts for the observed association

Continuum/spectrum Similar etiology; association is fairly specific and nonlinear

Precursor Similar etiology; predicts depression onset

Predisposition Predicts depression onset; other variables mediate or moderate this link

Pathoplasticity Predicts variation in presentation or outcome of depression above and beyond other baseline

characteristicsConcomitants Is altered during a depressive episode but returns to premorbid level after

Consequences/scars Is altered during and after a depressive episode

proposed (e.g., Akiskal et al. 1983, M.H. Klein

et al. 1993, Krueger & Tackett 2003). Theseproposed relations include: (a) personality and

depressive disorders have common causes;

(b) personality and depressive disorders forma continuous spectrum; (c) personality is a pre-

cursor of depressive disorders; (d) personalitypredisposes to developing depressive disor-

ders; (e) personality has pathoplastic effectson depression; (f) personality features are

state-dependent concomitants of depressiveepisodes; and (g) personality features are

consequences (or scars) of depressive episodes.The distinctions between some of these ac-

counts are subtle (cf. Kendler & Neale 2010),and other models, as well as combinations

of these scenarios, are plausible. However,

these seven models provide a useful conceptualframework for approaching the issue.

These models can be divided into threegroups. The first three models (common cause,

continuum/spectrum, and precursor) view per-sonality and depression as having similar causal

influences but do not see one as having acausal influence on the other. The fourth and

fifth models (predisposition and pathoplastic-ity) hold that personality has causal effects on

the onset or maintenance of depression.Finally,

the sixth and seventh models (concomitantsand consequences) view depression as having a

causal influence on personality. These models,and their unique predictions, are summarized

in Table 1.The common cause model views personality

and depressive disorders as distinct entities

that arise from the same, or at least an ove

lapping, set of etiological processes. From thperspective, personality and depression are n

directly related; rather, the association is du

to a shared third variable. The common caumodel would be supported by evidence th

personality traits and depression have sharetiological influences.

The continuum/spectrum model emphasizes the conceptual overlap betwe

depressive disorders and certain personaltraits and argues for a fundamental continui

between them. A depressive diagnosis thought to simply identify individuals w

have the most extreme scores on a releva

trait. Like the common cause model, tcontinuum/spectrum model assumes th

personality and depression arise from a similif not identical, set of causal factors. Howeve

the continuum/spectrum model goes furtherpositing that the association between the tr

and disorder should be fairly specific becauthey are on the same continuum.1 Moreov

this association is expected to be nonlineso that almost nobody below the definition

threshold on the trait has the diagnosis bnearly everyone above the threshold meets t

criteria. Thus, the continuum/spectrum mod

1There may not be complete specificity owing to diagnosheterogeneity. As discussed below, depression is a hetegeneous disorder with multiple etiological pathways (eqfinality). A personality trait may be part of only one of tpathways. In contrast, multifinality, in which the trait is sociated with multiple disorders, is less consistent with tcontinuum/spectrum view.



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would be supported by evidence that the trait

and depression are associated with the same eti-ological influences and that the trait-disorder

relationship is fairly specific and nonlinear.The precursor model views personality as

an early manifestation or forme fruste of de-

pressive disorder. Like the common cause and

continuum/spectrum accounts, the precursormodel posits that personality and depressivedisorders are caused by similar etiologic factors.

Also like the continuum/spectrum account, itimplies considerable phenomenologic similar-

ity between the relevant trait and depression.However, the precursor model differs from

both of these other models in that it assumesa particular developmental sequence, with the

personality traits being evident prior to the on-

set of depressive disorder. In other words, boththe common cause and continuum/spectrum

models assume a fixed clinical expression astraits or disorder, whereas the precursor model

implies escalation from traits to disorder withinindividuals over time. Support for theprecursor

model would come from evidence that the traitand depression are associated with the same

etiological influences and that individuals withhigh levels of the trait are at increased risk for

developing the disorder over time.2

The common cause, continuum/spectrum,

and precursor models do not posit causalrelations between personality and depression.

In contrast, the predisposition model holds that

personality plays a causal role in the onset ofdepression. However, the predisposition model

overlaps with the precursor model in that bothpropose that the relevant traits are evident prior

to the onset of depressive disorder. The majordifference between these two accounts is that

2

Applicationof the continuum/spectrumand precursor mod-els to depressive disorders is not straightforward. Person-ality traits are relatively stable, whereas depression is oftenepisodic. Existing formulations of the continuum/spectrummodel have not explained how stable trait characteristicsmanifest as an episodic illness. Similarly, the precursor modeldoes not account for why a stable trait would subsequentlydevelop into a nonstable depressive state. Thus, the contin-uum/spectrum and precursor models may provide a betterexplanation for chronic than episodic forms of depression.

Precursor modconsiders personan early manifesof the disorder

Predispositionmodel: posits tpersonality is difrom psychopatand plays a causin its developme

Pathoplasticitymodel: posits tpersonality influthe expression odisorder after on

the precursor model assumes that personality

and depression derive from the same set of etio-logical processes, but the predisposition model

posits that the processes that underlie person-ality differ from those that lead to depression.

Thus, the predisposition account implies a

complex interplay among risk factors involving

moderation and/or mediation, and this is whatdistinguishes it from the precursor model.3

The most common examplethe diathesis-

stress modelconceptualizes personality asthe diathesis and stress as a moderator that

precipitates the onset of depressive disorder.Alternatively, stress may be a mediator, so

that personality vulnerability leads to negativeexperiences (e.g., interpersonal rejection, job

loss), which in turn increase the probability

of a depressive episode. A second differencebetween these models is that the predisposition

model does not assume any phenomenologicallinks between personality traits and depressive

symptoms. Consequently, the predisposingtrait may not have any phenotypic similarity to

depression. Thus, the two most critical sourcesof support for the predisposition model would

involve demonstrating that individuals withthe trait are at increased risk for subsequently

developing depression, and that other variablesplay a role in mediating or moderating this

transition.

The pathoplasticity model is similar tothe predisposition model in that it also views

personality as having a causal influence ondepressive disorder. However, rather than con-

tributing to the onset of depression, the patho-plasticity model posits that personality influ-

ences the expression of the disorder after onset.This influence can include the severity or pat-

tern of symptomatology, course, and responseto treatment. The pathoplasticity model would

be supported by evidence that personality

3Although moderating and mediating variables play an ex-plicit and central role in the predisposition model, it shouldbe acknowledged that they are not incompatible with theprecursor account. That is, the escalation from personalitytraits to depressive disorders in the precursor model impliesthat additional variables (e.g., maturational or environmentalfactors) must be involved to precipitate the change.



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explains variation among depressed individuals

in their clinical presentation or outcome.The final two models also assume that there

is a causal relation between personality anddepression. However, these models reverse

the direction of causality. In the concomitants

(or state-dependent) model, assessments of

personality are colored, or distorted, by theindividuals mood state. This model impliesthat personality returns to its baseline form

after recovery from the episode. In contrast,the consequences (or scar) model holds that

depressive episodes have an enduring effect onpersonality, such that changes in personality

persist after recovery. These models would besupported by evidence that depression alters

levels of personality traits, either concurrently

(concomitants model) or over the longer-term(consequences model).

Dynamic Models ofPersonality-Depression Relations

The models above consider traits to be perfectlystable. As noted earlier, there is now extensive

evidence indicating that personality shows plas-ticity in childhood, with long-term test-retest

correlations of r 0.35, and continues tochange across the lifespan, although personality

consistency gradually increases up to r 0.75after the age of 50 (Roberts & DelVecchio

2000). Models of personality-psychopathologyrelations can be expanded to recognize the

malleability of traits (e.g., Ormel et al. 2001).

For example, one can posit a dynamic precursormodel4 in which early temperament defines the

baseline level of risk but subsequentexperiencesmodify personality liability to depression. This

model explains variability in disorder onset as afunction of the initial level of risk and steepness

of the trait trajectory over time. Given the evi-dence on patterns of personality continuity and

change (Roberts & DelVecchio 2000), it ap-

4This could also be called the dynamic continuum modelbecause once the dynamic element is introduced, it becomes

virtually impossible to distinguish the continuum/spectrumand precursor models.

pears likely that trait vulnerability is more m

leable early in life, but significant life events calter its trajectory even in old age. A depressi

disorder is thought to emerge when personalliability crosses the threshold. Thus, individ

als who are born with an elevated personali

liability or those with a rapidly increasing tr

trajectory would have a childhood onset of tdisorder, whereas those with a more slowincreasing trait trajectory would not cross th

threshold until much later, if ever. Moreovea pathological trait trajectory may be check

or reversed by positive experiences (Ormel de Jong 1999). In fact, personality genera

tends to change in a more adaptive directiowith age (Roberts et al. 2006), although th

pattern is not universal ( Johnson et al. 200

This may help to explain why the probabilityfirst-episode depression peaks in adolescenc

as trait deviance is more common at that ageSimilarly, the predisposition model can

expanded to recognizepersonality change. Thdynamic predisposition model (Ormel &

Jong, 1999, Ormel et al. 2001) acknowledgtransactions between personality and the env

ronment and integrates them with the enviromental moderation and mediation mechanism

of the classic predisposition model. In the envronmental moderation version of this accoun

negative life experiences influence not only d

pression onset but also levels of trait vulnerbility (Middledorp et al. 2008). This increase

personality liability may then lead to additionlife stress. If this vicious cycle is perpetuat

unchecked, personality liability would continto increase, and at some point, a negative li

event could overwhelm coping capabilities anelicit a depressive disorder. Importantly, and

contrast to thedynamic precursor model, in thaccount maladaptive traits alone are not suf

cient to cause depression, andan environmentrigger is necessary.

The vicious cycle of increasing trait vulne

ability and stress exposure does not necessarindicate that personality per se influenc

depression onset. Indeed, certain traits mincrease stress exposure but have no effect o

depression otherwise (e.g., it is possible that lo



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conscientiousness does not cause depression

directly but leads to depressogenic experiences,such as academic difficulties, job loss, and

relationship problems; Roberts et al. 2007),consistent with the environmental-mediation

pathway.

Dynamic models offerricher andmore com-

plete accounts of the role of personality in theonset of depression. Moreover, it is importantto recognizethatdepressive disorders havebeen

linked to multiple traits (as reviewed below),and it is likely that different personality charac-

teristics contribute through different pathways.

METHODOLOGICAL ISSUES

A number of methodological issues must beconsidered in evaluating the relation between

personality and mood disorders, including

(a) study design, (b) heterogeneity of depressivedisorders, and (c) assessment of personality.

Study Design

A number of research designs can be useful

in studying the relation between personalityand depressive disorders. The common cause,

continuum/spectrum, precursor, and predispo-sition models would all be supported by family

studies demonstrating personality differencesbetween nonaffected relatives of probands

with and without a history of depression. The

common cause, continuum/spectrum, and pre-cursor models would be supported by twin and

genetic association studies demonstrating thatthe same genes predispose to both personality

and depressive disorders. The precursor andpredisposition models posit that personality ab-

normalities are trait markers and hence shouldbe present prior to the onset, and after recovery

from, depressive episodes. Hence, these modelscan be tested by comparing individuals with a

history of depression that is currently in remis-

sion to persons with no history of depressionon relevant personality traits. An even stronger

approach to testing the precursor and predispo-sition models is to use prospective longitudinal

studies of persons with no prior history of

mood disorder to determine whether particular

personality traits predict the later onset ofdepressive disorder. Although no single design

can distinguish among these four models, thecombination of designs can bolster the case

for particular accounts. For example, finding

substantial common genetic variance in twin

studies, but no evidence of developmental se-quencing in longitudinal studies, wouldsupportthe common cause and continuum/spectrum

models. In turn, these two models could becompared by examining the specificity of the

association between trait and disorder andwhether there is a nonlinear relation between

trait level and probability of disorder. On theother hand, if there were evidence of develop-

mental sequencing in longitudinal studies as

well as substantial common genetic variancein twin studies (or overlap of other etiological

factors in other designs), it would support theprecursor model (particularly if the trait was

also phenomenologically similar to depression).In contrast, developmental sequencing but less

shared genetic (or other etiological) variancewould support the predisposition model. Also

crucial for the predisposition model is evidencefrom longitudinal studies demonstrating that

other variables (e.g., life stress) moderate ormediate the association between personality

and subsequent depression.

The pathoplasticity model can be evaluatedin longitudinal studies of persons with depres-

sive disorders by examining the associationsamong personality traits and clinical features,

course, and treatment response. Specifically,the pathoplasticity model posits that the trait

would predict these outcomes even aftercontrolling for initial illness severity and other

prognostic factors. Of note, an alternative ex-planation of such results is that the personality

trait is a marker for a more severe, chronic,

or etiologically distinct subgroup, rather thanhaving a causal influence on the expression

of the disorder. A multiwave follow-up ofindividuals with a depressive disorder could be

helpful in ruling out this possibility. If the traitinfluences the disorder course directly, rather

than because it is an indicator of a latent



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Dysthymic disorder:a condition defined bychronic but relativelymild feelings ofdepression lasting atleast two years

disorder class, changes in personality

scores should predict subsequent changes inoutcomes.

The concomitants model can be testedthrough cross-sectional studies comparing per-

sons who are currently depressed, persons who

have recovered from depressive episodes, and

healthy controls. An even better approach isto conduct longitudinal studies assessing indi-viduals when they are in a depressive episode

and again after they have recovered. If person-ality measures are abnormal during depressive

episodes but not after recovery, it would sug-gest that they are concomitantsof thedepressed

state. Multilevel analyses can also be used toseparate personality variance into trait and state

components and to test whether state variance

is associated with concurrent measures of de-pression (e.g., Duncan-Jones et al. 1990).

The consequences (or scar) hypothesis canbe evaluated by assessing persons before and

after a first depressive episode. If personalitydeviance is much greater after the episode has

remitted, it would suggest that scarring hasoccurred.

Testing dynamic theories requires longitu-dinal data with at least three assessment points.

These assessments should measure relevantcontextual factors (e.g., life stress) in addition

to depression and personality to allow the ex-

amination of dynamic and transactional effects.Multilevel modeling and structural equation

modeling offer powerful approaches to evalu-ating such effects with longitudinal data.

Heterogeneity of DepressiveDisorders

The depressive disorders are almost certainlyetiologically heterogeneous, reflecting the con-

vergence of multiple developmental pathways.Hence, it is likely that the role of personality

factors and, as suggested above, the applicabil-

ity of different models of the relation betweenpersonality and depression differ for different

forms of depression. The current classificationsystem for depressive disorders is based on

clinical features and is a poor approximation of

etiological distinctions. Nonetheless, it is im

portant to consider whether the role of persoality varies as a function of the specific depre

sive diagnosis (e.g., major depressive disordedysthymic disorder), subtype (e.g., psychot

melancholic, atypical), and clinical characte

istics such as age of onset, recurrence, an

chronicity. Failure to take heterogeneity inaccount may obscure important personalitdepression associations. Conversely, perso

ality may provide a basis for identifying mohomogeneous subgroups within the depressi

disorders. Unfortunately,few studies of persoality and depressive disorders have attempt

to take this heterogeneity into account.It is important to note, however, th

associations between personality and speci

subtypes and clinical characteristics do nnecessarily indicate etiological heterogenei

Instead, they could reflect pathoplasticiin which personality influences sympto

presentation and/or course, but the primaetiological process is the same, or they could r

flect differential severity of subtypes that resuin quantitative differences in their trait profil

Finally, a significant source of heterogenein depression is comorbidity with other form

of psychopathology. Given the high rates comorbidity, particularly with the anxie

disorders, associations between personal

and depressive disorders may actually reflethe relation of personality with a co-occurrin

nonmood disorder. Indeed, personality may a third variable that explains broad patterns

comorbidity among many disorders. For example, recent hierarchical models of classificatio

posit that trait dispositions such as N/Naccount for much of the comorbidity betwe

depression and other disorders (Griffith et 2010, Kotov et al. 2007). Thus, it is importa

for researchers to consider whether trahave specific relations with depression ov

and above more general associations with t

broader group of internalizing disorders.

Assessment

Temperament/personality can be assessed u

ing a variety of methods, including self-repo



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inventories, semistructured interviews, infor-

mants reports, and observations in naturalis-tic settings and the laboratory. Unfortunately,

most of the literature examining the associa-tion between personality and depressive dis-

orders has assessed personality via self-report.

This is potentially problematic because self-

reports of personality can be complicated bycurrent mood state, limited insight, responsestyles, and the difficulty of distinguishing traits

from the effects of stable environmental con-texts (Chmielewski & Watson 2009). In addi-

tion, when the same individual provides infor-mation on both personality and depression, as

has been the case in almost all studies in thisarea, common method variance can inflate as-

sociations. Hence, there is a need for greater

use of informant report and observationalmeasures.

A second issue concerns the overlapbetween some personality constructs and

psychopathology (Lahey 2004). For example,many items on N/NE scales are similar to de-

pressive symptoms (Ormel et al. 2004b). Thiscan inflate associations between measures of

personality and depression. On the other hand,personality and symptom assessments usually

have different time frames, with trait scalesreflecting long-standing patterns and depres-

sion measures tapping more recent experiences

(e.g., past week, past month). This trait versusstate distinction parallels that between person-

ality and other related constructs. For example,measures of N/NE and negative affect have

nearly identical content but are distinguishedby their time frames (Watson 2000). Thus, the

degree to which this content overlap threatensthe validity of personality-psychopathology

research depends, at least in part, on theduration/chronicity of the disorders of interest.

The extent to which this is a concern also de-pendson ones modelof personality-depression

relations. From the continuum/spectrum per-

spective,personality and depression are variantsof the same phenomenon, so the two constructs

should overlap. In contrast, the predispositionmodel views personality and depression as

distinct domains, so from this perspective it

DSM-IV: Diagand Statistical Mof Mental Disord

Fourth Edition

is important to define and assess these sets of

constructs as independently as possible and tojudiciously delineate their time frames.

AFFECTIVE TEMPERAMENTS

The classical European descriptive psy-

chopathologists in the late-nineteenth andearly-twentieth centuries observed that manypatients with mood disorders, as well as

their relatives, exhibited particular patternsof premorbid personalities that appeared to

be attenuated versions of their illnesses. Forexample, Kraepelin (1921) described four

patterns of personality that he consideredthe fundamental states underlying manic-

depressive illness: depressive, manic, irritable,

and cyclothymic temperament. He believedthat these were precursors or rudimentary

forms of the major mood disorders. Schneider(1958) described similar types; however, he

viewed them as personality disorders that werenot necessarily related to the mood disorders.

Two variants of these types, cyclothymicdisorder and dysthymic disorder, are included

as mood disorder diagnoses in the Diagnostic

and Statistical Manual of Mental Disorders,

Fourth Edition (DSM-IV; Am. Psychiatr. Assoc.1994). However, these disorders are defined

as fairly severe conditions, with the criteria

emphasizing symptomatology rather thanpersonality traits. As a result, these categories

appear to be limited to the more severe,symptomatic manifestations of the affective

temperaments described by Kraepelin andSchneider (Akiskal 1989).

On the basis of Kraepelins and Schneidersdescriptions, Akiskal (1989) proposed formal

criteria for the affective temperament types,and he and his colleagues developed interview

and self-report measures of these constructsthat have been applied in a number of settings

and cultures (e.g., Akiskal et al. 2005). Akiskals

work also provided the basis for including de-pressive temperament as a personality disorder

in the DSM-IV appendix. Of the four affectivetemperament types, depressive temperament

has been the most systematically studied in



10/29

Major depressivedisorder (MDD):a conditioncharacterized byepisodes of depressedmood or loss of

interest or pleasurelasting at least twoweeks

relation to nonbipolar depressive disorders.

The terms depressive temperament, depres-sive personality, and depressive personality

disorder have been used interchangeablyin the literature to refer to the following

constellation of traits: introversion, passivity,

and nonassertiveness; gloominess, cheer-

lessness, and joylessness; self-reproach andself-criticism; pessimism, guilt, and remorse;being critical and judgmental of others; consci-

entiousness and self-discipline; brooding andgiven to worry; and feelings of inadequacy and

low self-esteem.Data on the nature of the relation between

depressive personality and depressive disordersare consistent with most of the causal models

described above, illustrating the complexity

of the associations between personality anddepression. The strongest support for the com-

mon cause and continuum/spectrum modelsderives from twin and family studies. In a large

twin study, rstavik et al. (2007) found that de-pressive personality and majordepressive disor-

der (MDD) shared substantial genetic variance,although there was evidence for unique genetic

factors as well. Family studies indicate thatindividuals with depressive personality have an

increased rate of mood disorders in their first-degree relatives (e.g., Klein & Miller 1993).

In addition, patients with MDD, particularly

those with chronic forms of depression, haveelevated levels of depressive personality traits

in their first-degree relatives (Klein 1999).Consistent with Kraepelins (1921) retro-

spective observations, prospective longitudinaldata indicate that depressive personality traits

precede theonsetof depressive disorders.Kwonet al. (2000) found that young women with de-

pressive personality and no comorbid Axis Iand II disorders had a significantly increased

risk of developing dysthymic disorder (but notMDD) over the course of a three-year follow-

up. Taken together with the twin and family

studies, these findings provide compelling sup-port for the precursor model. In addition, in

light of the conceptual issue regarding traitsandstates raised above for the continuum/spectrum

and precursor models, it is noteworthy that

depressive personality is most closely associat

with chronic forms of depression at both tfamily and individual levels.

Evidence also supports the predispositio

pathoplasticity, and consequences modeRudolph & Klein (2009) reported that you

with elevated levels of depressive personal

traits experienced a significant increase depressive symptoms 12 months later. Whconsistent with the precursor model, it is not

worthy that this association was moderatby pubertal status and timing. Thus, you

with elevated levels of depressive personaltraits and more advanced pubertal stat

and earlier pubertal timing experienced tgreatest increase in depressive symptoms. Th

supports the predisposition model, suggesti

that depressive personality traits confer vulneability to depression in the presence of oth

maturational and psychosocial processes.Depressive personality also appears to ha

a pathoplastic effect on the course of depresive disorders, predicting poorer outcomes an

response to treatment (Laptook et al. 200Ryder et al. 2010). Moreover, Rudolph & Kle

(2009) recently reported preliminary suppofor the consequences model, at least in yout

They found that in a sample of early adlescents, higher levels of depressive symptom

predicted an increase in depressive personali

traits 12 months later. Finally, the limited eidence available suggests that semi-structur

interview assessments of depressive personalitraits are not influenced by a depressive episo

(Klein 1990), arguing against the concomitanmodel.

Although the work on affective tempeaments is important in understanding t

development of depressive disorders, it unlikely that these types actually reflect bas

temperamental processes that originate

early childhood, as their defining featurinclude a number of developmentally compl

cognitive and interpersonal characteristiInstead, these temperament types are mo

likely to be intermediate outcomes that reflethe interaction of more basic temperame

traits that are elaborated over development



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conjunction with early socialization and other

environment influences.In recent years, considerable evidence

has accumulated indicating that depressivepersonality is associated with several of the

basic personality trait dimensions discussed

below, particularly high N/NE and low E/PE

and a number of their facets (e.g., Huprich2003, Vachon et al. 2009).

PERSONALITY TRAITDIMENSIONS

The affective temperaments are conceptualized

within a categorical framework. In contrast,most of the other work on personality and

depression views personality in dimensionalterms. In this section, we focus on the FFM,

but we also briefly consider Grays (1994) and

Cloninger and colleagues (1993) psychobi-ological models and several additional traits

from the clinical literature (e.g., self-criticism,dependency, and rumination). This section

focuses primarily on studies of adults andadolescents using self-report measures of

personality. Studies of younger children usingobservational measures of temperament are

reviewed in a later section.

The Five-Factor Model

Cross-sectional associations. In their influ-

ential theory of personality and depression,Clark & Watson (1999, Clark et al. 1994)

posited that depressive disorders are character-ized by high levels of N/NE and low levels of

E/PE. A large number of cross-sectional stud-ies have evaluated these relations as well as the

links between depression and the other FFMdimensions. Kotov et al. (2010) recently con-

ducted a meta-analysis of this literature, whichrevealed that MDD is associated with very high

N/NE (Cohens d = 1.33) and low conscien-

tiousness (d = 0.90). The link to low E/PEwas more modest (d = 0.62) and inconsis-

tent, with some studies finding positive effects.The associations with the other two traits were

weak and unremarkable. The N/NE finding is

consistent with expectations, but the effect for

E/PE was smaller and that for conscientious-nesswas larger thananticipated. Dysthymicdis-

order exhibited a more extreme profile with re-markably strong and consistent links to E/PE

(d = 1.47), N/NE (d = 1.93), and conscien-

tiousness (d = 1.24). This is not surprising

as dysthymic disorder is thought to be moretrait-like than MDD, and a greater contribu-tion from personality might be expected.

To determine whether the observed per-sonality links are specific to depression, Kotov

et al. (2010) also examined personality profilesof anxiety disorders. They found that with the

exception of specific phobia, which had rela-tively weak associations with all five traits, all

anxiety disorders showed stronger effects on

N/NE, E/PE, and conscientiousness (averaged = 1.91, 1.05, 1.02, respectively) than did

MDD. Several also scored above dysthymic dis-order on N/NE. Dysthymia had stronger asso-

ciations than anxiety disorders on the other twotraits, but the differences were slight.

It is conceivable that more specific associ-ations were not evident because these analyses

focused on broad personality dimensions.Narrow traits that comprise the general di-

mensions may have stronger associations withdepressive disorders. Indeed, self-harma

component of N/NE that reflects propensity to

self-deprecation and self-injurywas found tocontribute to depression even after controlling

for the broad traits, and this effect was specificrelative to other common mental disorders

(Watson et al. 2006). With regard to E/PE,evidence is emerging that the positive affec-

tivity facet, but not the sociability/extraversionfacet, is related to depression (Durbin et al.

2005, Naragon-Gainey et al. 2009). This mayexplain the surprisingly modest association

between MDD and E/PE, if this general

trait includes much variance not relevant todepression. Thus, facet-level research promises

to yield stronger and more specific evidence ofpersonality-depression links.

Evidence bearing on causal models. Be-

cause most attempts to tease apart explanatory



12/29

models of the association between depression

and personality have focused on N/NE andE/PE, we consider only these two traits in this

section. The section is organized by the type ofresearch design used to address the models.

Personality during and after a depres-

sive episode. Studies of personality and psy-chopathology may be complicated by the in-fluence of participants mood states on reports

of their personalities (the concomitants model).For example, many studies have found that in-

dividuals with MDD report higher levels ofN/NE when they are depressed than when

they are not depressed (Hirschfeld et al. 1983b,Kendler et al. 1993, Ormel et al. 2004a). In

contrast, the evidence for mood state effects on

E/PE is weaker and less consistent (de Fruytet al. 2006, Kendler et al. 1993, Morey et al.

2010). However, the influence of mood stateon personality should not be overstated. Even

though levels of N/NE decline significantly af-ter remission from a depressive episode (i.e.,

absolute stability), individuals relative posi-tions with respect to levels of N/NE (i.e., rank-

order stability) tend to be moderately well pre-served (de Fruyt et al. 2006, Morey et al. 2010).

Moreover, clinical trials suggest that changesin depressive symptoms are not necessarily ac-

companied by changes in personality (Quilty

et al. 2008b, Tang et al. 2009).

Cross-sectional comparisons of remitted pa-

tients and controls. A number of early stud-

ies used remission designs, comparing patientswho had recovered from a depressive episode to

never-depressed controls or population normson self-rated personality traits. These studies

found that E/PE is significantly lower in for-merly depressed patients than in healthy con-

trols (Hirschfeld et al. 1983a, Reich et al. 1987),arguing against the concomitants model and in

favor of the precursor, predisposition, and/or

consequences models. However, the results forN/NE were less consistent (Hirschfeld et al.

1983a, Reich et al. 1987). This inconsistencymay be due to a number of factors, includ-

ing insufficiently stringent criteria for recovery,

thereby possibly confounding personality an

residual symptoms; using normative data colected by other investigators, which may intr

duce demographic and sociocultural differenc

between the formerly depressed and comparson samples; and selection effects, as N/NE

associated with a poorer course (discussed b

low) and thus samples of remitted depressivmay include a disproportionate number wilow levels of this trait.

Personality before and after a depressi

episode. Several studies have tested the consquences (or scar) hypothesis by comparing pe

sonality measures in depressed individuals bfore and after a MDD episode. The results

these studies have been inconsistent. Kendl

andcolleagues reported increasesin N/NE (bnot E/PE) after a depressive episode in tw

separate samples (Fanous et al. 2007, Kendlet al. 1993); however, other studies have foun

that N/NE and E/PE do not change from bfore to after a MDD episode (e.g., Ormel et

2004a, Shea et al. 1996). Importantly, the stuies reportingscarring used less stringentcriter

for recovery and shorter follow-ups, suggestithat the findings may be due to residual sym

toms and/or that the scars dissipate over tim

Personality in relatives of depressed ind

viduals. A number of studies have tested tcommon cause, continuum/spectrum, precu

sor, and predisposition models by comparinpersonality traits in the never-depressed rel

tives of patients with mood disordersand nevedepressed controls (e.g., Farmer et al. 200

Hecht et al. 1998, Ouimette et al. 1996). Thresults have been mixed, with some studies r

porting higher N/NE and/or lower E/PE the never-depressed relatives of probands wi

mood disorders, and other studies reporting n

differences. However, interpretation of thestudies is complicated by two factors. First, pe

sonality traits may not play the same role risk for depression among familial as nonf

milial forms of depression. Second, there mbe selection biases in samples using well rel

tives who are already partly through the ri



13/29

period for mood disorder. Thus, those rela-

tives with the strongest personality vulnerabil-ities may have already developed the disorder

and be excluded from the study.

Twin studies. As discussed above, a valu-able approach to testing the common cause,

continuum/spectrum, and precursor models isthrough twin studies. These studies indicate

that there are substantial associations between

the liabilities for N/NE and MDD, but onlyweak associations between the genetic liabili-

ties for E/PE and MDD (Fanous et al. 2007;Kendler et al. 1993, 2006).

Prospective longitudinal studies. The most di-

rect approach to testing the precursor and pre-disposition models is to conduct prospective

studies of personality in never-depressed partic-ipants to determine whether personality char-

acteristics predict the subsequent onset of de-pressive disorders. Several studies using large

community samples have reported that higherlevels of N/NE predict theonset of first lifetime

MDD episodes (de Graaf et al. 2002; Fanous

et al. 2007; Kendler et al. 1993, 2006; Ormelet al. 2004a). In addition, several studies us-

ing measures of other traits that overlap withN/NE or its facets have reported similar find-

ings (Hirschfeld et al. 1989, Rorsman et al.1993). Although there is some evidence that

E/PE predicts the first onset of MDD (Kendleret al. 2006, Rorsman et al. 1993), it is much

weaker, and several studies have failed to findan association (Fanous et al. 2007, Hirschfeld

et al. 1989, Kendler et al. 1993).

Personality and the subsequent course of de-

pression. Finally, there is evidence that both

N/NE and E/PE have pathoplastic influenceson the course of depression after the onset of

the disorder. For example, many studies have

reported that higher N/NE and lower E/PEpredict a poorer course and response to treat-

ment, although thefindings regardingE/PE areslightly less consistent (de Fruyt et al. 2006,

Duggan et al. 1990, Morris et al. 2009, Quilty

et al. 2008a, Tang et al. 2009). As noted above,

however, these findings are also consistent withdiagnostic heterogeneity, such that personal-

ity dysfunction is a marker for a more severeor etiologically distinct group. Indeed, there is

evidence that the nonmelancholic subtype is

characterized by more vulnerable personality

styles than is melancholia and that chronic de-pressions are associated with higher N/NE andlower E/PE than is nonchronic MDD (Klein

2008, Kotov et al. 2010).

Evidence relevant to dynamic models.

Transactions between N/NE and environmen-

tal contexts have received the most attentionin the literature (Ormel & de Jong 1999, van

Os & Jones 1999). N/NE shows reciprocal

relations with a range of significant life expe-riences, such as initiation and break-up of a

committed relationship, relationship quality,occupational attainment, and financial security

(Neyer & Lehnart 2007, Roberts et al. 2003,Scollon & Diener 2006). Furthermore, N/NE

has been repeatedly implicated in the gen-eration of stressful life events (Kercher et al.

2009, Lahey 2009, Middeldorp et al. 2008),which suggests an environmentally mediated

relationship between this trait and depression.The environmentally moderated mechanism

has also received support, as several studies

found that N/NE interacts with stressful lifeevents to predict first onset of major depression

(Kendler et al. 2004, Ormel et al. 2001, van Os& Jones 1999).

E/PE has demonstrated bidirectional effectswith many significant social and occupational

experiences (Neyer & Lehnart 2007, Robertset al. 2003, Scollon & Diener 2006). In addi-

tion, a decrease in E/PE over time was foundto predict future internalizing problems (Van

den Akker et al. 2010). However, little atten-

tion has been given to mechanisms underlyingthe association between this trait and depres-

sion. Support for an environmentally mediatedeffect is limited and mixed (Middeldorp et al.

2008, Wetter & Hankin2009), andthe environ-mental moderation model is largely untested,

although there is some evidence that positive



14/29

affect moderates the effects of daily stressors on

depressive symptoms (Wichers et al. 2007).Finally, conscientiousness may play an im-

portant role in dynamic models of personality-depression relations. It has reciprocal associa-

tions with familysupport, divorce, occupational

attainment, and job involvement (Roberts et al.

2003, Roberts & Bogg 2004). Conscientious-ness is hypothesized to influence depressionby increasing exposure to negative life events

(Anderson & McLean 1997, Compas et al.2004), but mediation and moderation effects

have not been tested.

Interactions between temperament dimen-

sions. Finally, personality-depression rela-

tions may be multivariate, rather than bivariate,

with multiple traits interacting to influ-ence depression. Indeed, in their influential

model of personality and depression, Clark &Watson (1999, Clark et al. 1994) hypothesized

that depression is characterized by high N/NEand low E/PE, raising the possibility that it is

the combination of thetwo traits that is particu-larly important in depressive disorders. A grow-

ing number of studies have reported that the in-teraction of high N/NE and low E/PE predicts

subsequent depressive symptoms or disordersin adults and youth (Gershuny & Sher 1998,

Joiner & Lonigan 2000, Wetter & Hankin

2009), although several studies have not foundsuch an interaction (Jorm et al. 2000, Kendler

et al. 2006, Verstraeten et al. 2009). The inter-action between N/NE and conscientiousness is

also of interest, as the latter construct includesaspects of self-regulation and effortful control

(Rothbart & Bates 2006) and may therefore re-flect the ability to modulate ones affective reac-

tivity. Indeed, there is cross-sectional evidencethat effortful control moderates the association

between N/NE and depressive symptoms inadolescents (Verstraeten et al. 2009).

Summary and discussion. Cross-sectionalstudies have documented strong links of

depressive disorders to N/NE, conscien-tiousness, and E/PE, although the latter

effect is substantial in dysthymic disorder but

only moderate in MDD. In fact, personali

generally appears to play a greater role dysthymia. None of these relations are specifi

however, as anxiety disorders have very simil

trait profiles. This observation argues againthe continuum/spectrum model at least wi

regard to these broad dimensions. It may

possible to find traits that are specific to dpression by targeting lower-order personalidimensions. Narrower traits may also expla

the surprisingly modest link between E/PE aMDD, as some, but not other, facets of th

general dimension are relevant to depressionThe nature of relations between the

personality traits and depression is compleand our understanding is still limited. N/N

the most widely studied personality trait

depression, raises challenging conceptual anmethodological issues due to the overl

between some of its features and depressisymptoms (Ormel et al. 2004b). Nonethele

this cannot completely explain the associatibetween these constructs (Tang et al. 2009

N/NE is moderately influenced by clinical sta(the concomitants model), shares comm

etiological influences with MDD (commcause, continuum/spectrum, and precurs

models), predicts the subsequent onset MDD (precursor and predisposition model

and influences the course of depression (path

plasticity model). In addition, N/NE appeato contribute to subsequent stress and adversi

and increases the risk of depression in the faof negative life events (predisposition mode

Finally, it may also be changed by experienceMDD episodes (consequences model), but t

evidence for this is weaker and less consistenThe role played by E/PE in depression is le

clear. Its cross-sectional association with dythymia is substantial, but its relation to MDD

more modest. E/PE is not influenced by clini

state or changed by the experience of depresive episodes. It appears to be abnormally lo

even during remission, which is consistent withe continuation of trait deviance from the pr

morbid stage (precursor or predisposition acounts). Moreover, low E/PE tends to predi

a poorer course of depression. However, t



15/29

degree of shared etiological influences between

E/PE and MDD is low, and the evidence thatE/PE predicts theonset of MDD in prospective

longitudinal studies is weak. As noted above,three possible reasons for the weaker and less

consistent findings regarding E/PE are (a) it

plays a greater role in some forms of depres-

sion than others (e.g., chronic depressions);(b) only some facets of the broader trait (e.g.,low positive affective and approach motivation)

are related to depression; and (c) E/PE maymake a greater contribution to depression by

moderating N/NE than as a main effect (Olinoet al. 2010).

Finally, there appears to be a strong negativeassociation between conscientiousness and de-

pression, at least in cross-sectional studies. This

may appear surprising in light of the positiveassociations discussed below between depres-

sion and a number of other constructs thatare thought to be related to conscientiousness,

such as behavioral inhibition system sensitivity,harm avoidance, perfectionism, and temper-

amental behavioral inhibition. It is importantto note, however, that these latter constructs

are more strongly associated with high N/NE,and in some cases, low E/PE, than with consci-

entiousness (de Fruyt et al. 2000, Muris et al.2009a, Smits & Boeck 2006). Hence, it is likely

that their positive correlations with depression

are driven by their shared variance with highN/NE. Unfortunately, few studies testing

causal models of personality and depressionhave considered conscientiousness. However,

evidence indicating that this trait may mod-erate the effects of N/NE on depression and

that it increases the likelihood of subsequentadversity that could then, in turn, produce

depression suggests that further research onthe role of conscientiousness is warranted.

Psychobiological Models

Grays model. Grays (e.g., Gray 1994) influ-ential theory proposes that there are two major

neurobehavioral systems that underlie behav-ior: the behavioral activation system (BAS),

which responds to signals of reward, and the be-

BAS: behavioraactivation system

BIS: behaviorainhibition system

havioral inhibition system (BIS), which is sensi-

tive to cues for punishment. Although BAS andBIS differ conceptually and empirically from

E/PE and N/NE, their relations with depres-sion are thought to be similar. Thus, it has been

hypothesized that depression is associated with

reduced BAS and/or heightened BIS sensitivity

(Depue & Iacono 1989, Gray 1994). Althoughmuch of this work has focused on bipolar disor-der (e.g., Alloy et al. 2008, Johnson et al. 2008),

several recent studies have examined self-reportmeasures of BAS and BIS sensitivity in MDD.

Consistent with Grays model, compared withhealthy controls, currently depressed patients

report lower levels of BAS and higher levels ofBIS, and patients with a past history of MDD

report lower levels of BAS (Pinto-Meza et al.

2006). In addition, lower BAS sensitivity, butnot higher BIS sensitivity, is associated with a

poorer course of MDD (e.g., Kasch et al. 2002,McFarland et al. 2006), suggesting that BAS

may have a pathoplastic effect on depression.

Cloningers model. Cloninger (e.g.,Cloninger et al. 1993) has proposed a

model of personality that includes four tem-perament and three character dimensions.

The temperament dimensions include noveltyseeking (an appetitive/approach system), harm

avoidance (an inhibition/avoidance system),

reward dependency (a system that is responsiveto signals of social approval and attachment),

and persistence. The character dimensions areself-directedness (responsible, goal-directed),

cooperativeness (helpful, empathic versushostile and alienated), and self-transcendence

(imaginative, unconventional). Harm avoid-ance is conceptually and empirically associated

with BIS, and novelty seeking and persis-tence are associated with BAS. Similarly,

harm avoidance is positively correlated withN/NE and negatively associated with E/PE,

self-directedness is negatively correlated with

N/NE, and novelty seeking and persistenceare associated with E/PE (e.g., de Fruyt et al.

2000).A number of studies have reported that pa-

tients with MDD report higher levels of harm



16/29

avoidance and lower levels of self-directedness

than do healthy controls (e.g., Celikel et al.2009). Most of the traits in Cloningers system

are influenced by the respondents mood state(e.g., Farmer et al. 2003); however, abnormal

levels of harm avoidance and self-directedness

are present even after remission (e.g., Smith

et al. 2005). Increased harm avoidance andlower self-directedness are also characteristicof most anxiety disorders, indicating that these

effects are not specific to MDD (Ongur et al.2005).

Few studies have explicitly tested the com-mon cause, precursor, predisposition, and con-

sequences hypotheses for Cloningers model.Farmer et al. (2003) found that the never-

depressed siblings of patients with MDD re-

ported significantly greater harm avoidanceand less self-directedness than did the never-

depressed siblings of healthy controls. In addi-tion, Cloninger et al. (2006) reported that in a

large community sample, high harm avoidanceand persistence and low self-directedness pre-

dicted an increase in self-reported depressivesymptoms 12 months later. A larger number of

studies have addressed the pathoplasticity hy-pothesis, albeit with mixed results. Low harm

avoidance, self-directedness, and reward de-pendency have predicted a poorer response to

treatmentin some, but not all, studies; theother

dimensions have generally not been associatedwith course and treatmentoutcome ( Joyce et al.

2007, Kennedy et al. 2005, Morris et al. 2009).

Clinical Traits

Independent of the traditional personality field,clinical researchers have developed a number of

trait-like constructs to describe dispositions todepression. These clinical traits are similar in

scope to personality facets, and their stability iscomparable to that of a typical personality di-

mension (e.g., Kasch et al. 2001, Zuroff et al.

2004). Also, factor analytic studies have shownthat most of these clinical traits can be success-

fully incorporated in the personality taxonomyas components of neuroticism (Watson et al.

2006). Next, we brieflydiscuss threeof themost

studied constructs: ruminative response sty

self-criticism, and dependency.Ruminative response style, a tendency

dwell on sad mood and thoughts (NoleHoeksema 1991), is correlated with concurre

depressive symptoms and predicts future sym

toms as well as increases in symptoms over tim

(Rood et al. 2009). Also, one study reportthat ruminative response style prospectivepredicts onset of MDD (Nolen-Hoeksem

2000). The trait has also been linked to anxiedisorders, but the association with depressio

is appreciably stronger (Cox et al. 200Nolen-Hoeksema et al. 2008).

Blatts (1974, 1991) theory of depressiofocuses on two trait vulnerabilities: se

criticism (an inclination to feelings of gu

and failure stemming from unrealistically hiexpectations for oneself) and dependency

disposition to feelings of helplessness and feaof abandonment resulting from a preoccup

tion with relationships). These constructs asimilar, although not identical, to Becks (198

constructs of autonomy and sociotropy. Studindicate that the link between dependen

and depressive disorders is relatively weak annonspecific, whereas self-criticism has be

established as an important and specific factin these conditions (Zuroff et al. 2004). Bo

traits have been conceptualized as dynam

predispositions to depressive disorders, athere is some support for this view, includin

evidence of transactions with life stress as was environmental mediation and moderati

of personality effects (Zuroff et al. 2004). Secriticism, and to a lesser extent dependenc

have also been found to predict future increasin depressive symptoms. In addition, there

evidence that dependency predicts the subsquent onset of major depression in older, b

notyounger, individuals (Hirschfeld et al. 198Rohde et al. 1990). The concomitants a

pathoplasty models have also received empir

cal support (Zuroff et al. 2004). Finally, theresome research indicating that dependency m

increase as a function of depressive episod(consequences model) in youth but not adu

(Rohde et al. 1990, 1994; Shea et al. 1996).



17/29

As noted above, all of these constructs are

stronglylinkedtoN/NE(Coxetal.2001,Kaschet al. 2001), and some (particularly rumination

and self-criticism) can be considered facets ofthis broader trait (Watson et al. 2006). Lower-

order facets can account for variance over and

above that of higher-order traits (Paunonen

& Ashton 2001), and several cross-sectionalstudies have supported the incremental validityof ruminative response style and self-criticism

(Cox et al. 2004, Muris et al. 2009b) in associa-tions with depressive symptoms. However, this

issue requires more research, particularly usinglongitudinal designs.

CHILD TEMPERAMENT

Most of the literature on personality and de-

pression has focused on adolescents and adults.

Research that is grounded in the child temper-ament literature in developmental psychology

has the potential to extend existing work onpersonality in depression by (a) providing the

strongest test of the precursor and predisposi-tion models; (b) more precisely delineating the

behavioral manifestations of temperamentalvulnerabilities to mood disorders in young

children; (c) tracing the development and conti-nuity of trait vulnerabilities across the lifespan;

and (d) examining the neurobiological, cog-nitive, and interpersonal processes that may

mediate the association between early tempera-

ment traits and the subsequent development ofdepressive disorder (Compas et al. 2004, Klein

et al. 2008a, Kovacs & Lopez-Duran 2010).The early childhood temperament dimen-

sions that have received the greatest attentionwith respect to depression are N/NE, E/PE,

andbehavioral inhibition (BI). BI refersto wari-ness, fear, and low exploration in novel situa-

tions (Kagan et al. 1987). It combines aspectsof N/NE (fear and anxiety), E/PE (low ap-

proach), and conscientiousness (constraint/ ef-

fortful control) that do not have a direct analogin most models of adult personality.

Cross-sectional and longitudinal studies ofolder children and adolescents using self-report

measures have generally reported associations

BI: behavioralinhibition

of low E/PE and high N/NE with depression

similar to those in the adult literature (e.g.,Lonigan et al. 2003).5 Observational studies of

younger children of depressed mothers also in-dicate that these traits may be associated with

risk for depression (Kovacs & Lopez-Duran

2010). For example, in a community sample of

100 three-year-olds, Durbin et al. (2005) re-ported that children of mothers with a historyof mood disorder exhibited low PE in emotion-

eliciting laboratory tasks. Importantly, this ef-fect was limited to the affective (positive af-

fect) and motivational (approach/engagement),rather than the interpersonal (sociability), com-

ponents of PE. Furthermore, low PE at age3 predicted depressotypic cognition and mem-

ory biases at age 7 (Hayden et al. 2006) and

parent-reported depressive symptoms at age 10(Dougherty et al. 2010).

Subsequently, using a larger communitysample (N = 543), Olino et al. (2010) found

that preschool-aged children of parents with ahistory of depression had higher levels of NE

and BI. However, both main effects were qual-ified by interactions with child PE. At high

and moderate (but not low) levels of child PE,higher levels of NE and BI were each associ-

ated with higher rates of parental depression.Conversely, at low (but not high and moder-

ate) levels of child NE, low PE was associated

with higher rates of parental depression. Takentogether, these results suggest that children of

depressed parents may exhibit diminished PEor elevated NE and BI. In this latter sample,

low PE was also associated with elevated levelsof cortisol shortly after awakening, an index of

hypothalamic-pituitary-adrenal axis dysregula-tion that has been shown to predict MDD in

adolescents and adults (Dougherty et al. 2009).In both the Durbin et al. (2005) and Olino

et al. (2010) studies, the child temperamentparental psychopathology associations were

5Few studies have examined the association of conscientious-ness/effortful control with depression in youth, but analo-gous to the adult literature, there is cross-sectional evidencethat effortful control is negatively correlated with depression(Verstraeten et al. 2009).



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specific to depression. However, other work

suggests that children of parents with anxietydisorders may also exhibit elevated BI. For ex-

ample, Rosenbaum et al. (2000) assessed BI us-inglaboratorymeasuresin2-to6-year-oldchil-

dren of parents with a history of MDD and/or

panic disorder and parents with no history of

mood or anxiety disorders. Children of patientswith both MDD and panic disorder exhibitedsignificantlygreater BI than did children of par-

ents with no history of mood or anxiety dis-order. Children of parents with panic disor-

der alone and children of parents with MDDalone had intermediate levels of BI that did

not differ significantly from children of par-ents in the comorbid and no-psychopathology

groups.

Finally, there is some direct evidence thatpersonality traits assessed in childhood predict

the development of depressive disorders inadults. Caspi et al. (1996)reported that children

who were rated as socially reticent, inhibited,and easily upset at age 3 had elevated rates of

depressive (but not anxiety or substance use)disorders at age 21. Moreover, van Os et al.

(1997) found that physicians ratings of behav-ioral apathy at ages 6, 7, and 11 were predictive

of both adolescent mood disorder and chronicdepression in middle adulthood. However, BI

appears to predict the development of anxiety

disorders at least as strongly as depression(Hirshfeld-Becker et al. 2008).

CLINICAL IMPLICATIONS

Prevention

Personality researchhas importantimplications

for the prevention of depression. Meta-analyticevidence indicates that existing preventive

interventions can reduce the incidence of de-pressive disordersby 25%(Cuijpers et al. 2008).

However, the available strategies are a mix of

universal (intervention is administered to theentire population), selective (to a well-defined

at-risk group), and indicated (to those withsubthreshold disorder) approaches. Universal

interventions are costly, lack a personalized

focus, and require very large samples to yie

detectable effects, whereas indicated intervetions may be better described as treatment th

prevention (Munoz et al. 2010). In contraselective interventions are true preventi

measures that are cost effective and can

tailored to a specific mechanism of risk. How

ever, implementation of selective strategrequires knowledge of risk factors and causprocesses that lead from the vulnerability to t

disorder.The majority of established risk factors f

depressive disorders are either immutable (e.demographic characteristics, family history)

predict onset only in theshort term (e.g., streful lifeevents). In contrast, personality is at le

somewhat malleable, especially in youth, b

may forecast the onset of depression years advance, which makes traitsa potentially attra

tive means of identifying individuals at risk aninforming selection of interventions. Differe

trait-disorder pathways wouldpoint to differepreventive strategies; hence, further resear

on the nature of personality-depression reltions can significantly facilitate developme

of preventive interventions. Another advantaof traits is that they can be assessed relative

easily and efficiently and thus are ideal fscreening.

Treatment Response

Personality also can inform treatment depressive disorders post onset. In particula

traits can predict response to treatmenSubstantial evidence has accumulated th

individuals with lower N/NE have better treament outcomes across modalities (Kenne

et al. 2005, Mulder 2002, Tang et al. 2009Other Big Five traits have been studied less a

their role is not yet certain. However, a recelarge investigation of a combination interve

tion (medication plus psychotherapy) foun

that low N/NE and high conscientiousnepredicted who would respond to treatme

and although high E/PE did not contribudirectly, it amplified the effect of high consc

entiousness (Quilty et al. 2008a). As discuss



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above, investigations of Cloningers traits have

produced inconsistent results ( Joyce et al.2007, Kennedy et al. 2005, Mulder 2002). Few

studies have examined personality facets, butpreliminary evidence suggests that lower-order

traits can add substantially to the prediction of

treatment response (Bagby et al. 2008). Among

clinical traits, self-criticism, but not depen-dency, was found to forecast poor treatmentoutcomes (Blatt et al. 1995). Furthermore, per-

sonality may be useful in matching patients tointerventions. For instance, Bagby et al. (2008)

reported that patients high on N/NE or low onsome agreeableness facets respond better to an-

tidepressant medication than to psychotherapy.The processes underlying these predictive

associations are not entirely clear. One hypoth-

esis is that personality change mediates the ef-fect of treatment on depression. Indeed, there

is a fair amount of evidence that depressiontreatment reduces N/NE and increases E/PE

(Zinbarg et al. 2008) and that this effect isnot due to confounding by the depressive state

(Tang et al. 2009). Quilty et al. (2008b) tested amediation model and found direct support for

this hypothesis. Other possibilities need to beruled out, however, particularly the hypotheses

that traits predict poorer response because theyindicate a more severe form of depression or

that they interfere with treatment compliance

and the therapeutic relationship, thus reducingthe efficacy of the intervention.

CONCLUSIONS AND FUTUREDIRECTIONS

The literature on the relation between person-ality and depression is large, but it has many

gaps and inconsistent findings. Nonetheless,it is possible to draw a number of conclu-

sions. First, there are moderate-to-large cross-sectional associations between depression and

three general personality traitsN/NE, E/PE,

and conscientiousnessas well as with a vari-ety of related traits (e.g., harm avoidance, ru-

mination, and self-criticism) and personalitytypes (depressive personality). Second, most of

the personality traits associated with depression

also are related to other forms of psychopathol-

ogy,particularly anxiety disorders.Thismay re-flect the phenomenon of multifinality, in which

variables early in the causal chain lead to multi-ple outcomes depending on subsequent events

in the causal pathway. On the other hand, many

of the disorders that are currently classified as

distinct conditions are closely related; hence,research on personality-psychopathology asso-ciations can provide important information for

revising our nosological system. Third, reportsof some traits (e.g., N/NE and harm avoidance)

are influenced by clinical state, whereas othertraits (e.g., E/PE) appear to be independent of

mood state. However, state effects cannot fullyaccount for the associations between person-

ality and depression. Fourth, shared etiologi-

cal factors (e.g., genes) account for a portion ofthe association between N/NE and depression.

Fifth, depressive personality and some traits,particularly N/NE, predict the subsequent on-

set of depressive disorders. However, it is un-clear at this point whether they are best con-

ceptualized as precursors or predispositions, asit is difficult to tease these models apart, and

there is evidence supporting both accounts.In either case, there is growing evidence that

temperamental risk factors are evident at anearly age, suggesting a promising approach to

identifying young children at risk for depres-

sion. Sixth, there is evidence suggesting thatother traits, such as low E/PE and low con-

scientiousness/effortful control, may moderatethe relationship between N/NE and depres-

sion. Seventh, it appears unlikely that depres-sive episodes produce enduringchanges in most

personality traits. Finally, personality traits pre-dict, and may in fact influence, the course and

treatment response of depression.To make further progress in elucidating the

relation between personality and mood disor-ders, future studies should be guided by six

broad considerations. First, most of the litera-

ture on personality and depression has focusedon the broad traits of N/NE and E/PE. There

is a need for further work on conscientiousnessand on lower levels in the trait hierarchy (i.e.,

facets). It is important to determine whether a



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more specific level of analysis will yield more

powerful effects and increase the specificity ofassociations between personality constructs and

particular forms of psychopathology. Clinicaltraits, such as ruminative response style and

self-criticism, need to be included in these stud-

ies and evaluated jointly with traditional per-

sonality dimensions. Finally, it is importantto continue to explore interactions betweentraits.

Second, there is a critical need for prospec-tive, longitudinal studies. Most existing longi-

tudinal studies have begun in late adolescenceor adulthood. However, a substantial propor-

tion of mood disorders have already developedby mid-adolescence. Therefore, in order to fur-

ther test the precursor and predisposition mod-

els, and to trace the developmental pathwaysbetween personality and depression, it is neces-

sary to conduct longitudinal studies that start asearly as possible in order to obtain a sufficient

number of first-onset cases and avoid selectionbiases caused by excluding participants who al-

ready have a history of mood disorder at initialassessment.

Third, depression researchers have treatedpersonality as static. However, personality

changes over the course of development.Future work must begin to consider the

complex personality-environment transactions

that can strengthen or attenuate personalitytrajectories and predispositions for depressive

disorder. In addition, as understanding ofepigenetics increases, it will be important to

explore epigenetic influences on personal

change and their relation to depression.Fourth, if personality is a precursor of,

predisposes to, the development of depressidisorders, it is critical to identify the modera

ing factors and mediating processes involved

these pathways. There is some evidence su

gesting that moderators may include gendeearly adversity, and life stress, and mediatomay include interpersonal deficits, depress

typic cognitions, maladaptive coping, and bhavioral and neurobiological stress reactivi

(Klein et al. 2008a). There is a need for mosystematic research examining these modertors and mediators in a longitudinal framewor

Fifth, self-reports have borne the brunt most research in this area andhave made impo

tant contributions. However, like all methodthey have limitations and cannot be applied

all contexts (e.g., young children). Thus, theis a need for further work using complementa

methods such as informant reports and obsevations in naturalistic and laboratory settings

Finally, therole of personality/temperamemay differ for different forms of depressive d

order. Personality appears to play an especia

important role in early-onset, chronic, and rcurrent depressive conditions (e.g., Klein 200

Kotov et al. 2010, van Os et al. 1997). Focusinon broad diagnostic categories such as MD

mayobscure importantassociations withpartiular forms of depression; hence, future studi

need to give greater consideration to the heerogeneity of depressive disorders.

SUMMARY POINTS

1. There are moderate-to-large cross-sectional associations between depression and threegeneral personality traitsN/NE, E/PE, and conscientiousnessas well as with a variety

of related traits (e.g., harm avoidance, rumination, and self-criticism) and personality

types (e.g., depressive personality).

2. Most of the personality traits associated with depression also are related to other forms

of psychopathology, particularly anxiety disorders. This may reflect the phenomenonof multifinality, in which variables early in the causal chain lead to multiple outcomes

depending on subsequent events in the causal pathway. On the other hand, many of the



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disorders that are currently classified as distinct conditions are closely related; hence,research on personality-psychopathology associations can also provide important infor-

mation for revising our nosological system.

3. Reports of some traits (e.g., N/NE and harm avoidance) are influenced by clinical state,

whereas other traits (e.g., E/PE) appear to be independent of mood state. However, stateeffects cannot fully account for the associations between personality and depression.

4. Shared etiological factors (e.g., genes) account for a portion of the association between

N/NE and depression.

5. Depressive personality and some traits, particularly N/NE, predict the subsequent

onset of depressive disorders. However, it is unclear at this point whether they are

best conceptualized as precursors or predispositions, as it is difficult to tease thesemodels apart, and there is evidence supporting both accounts. In either case, there is

growing evidence that temperamental risk factors are evident at an early age, suggestinga promising approach to identifying young children at risk for depression.

6. There is evidence suggesting that other traits, such as low E/PE and

Personalidad y Depresion

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