Internalizing problems of childhood and adolescence ... · problems. There also tends to be less...

Development and Psychopathology, 12 (2000), 443–466Copyright 2000 Cambridge University PressPrinted in the United States of America

Internalizing problems of childhood andadolescence: Prospects, pitfalls, and progressin understanding the development of anxietyand depression

CAROLYN ZAHN–WAXLER, BONNIE KLIMES–DOUGAN, AND

MARCIA J. SLATTERYNational Institute of Mental Health

AbstractThe focus of this article is on internalizing problems that are experienced by children and adolescents. We providean historical perspective, selectively examine the current state of knowledge, consider advances and gaps in what isknown, and identify new research directions. Diagnosis, epidemiology, theory, and research first are consideredseparately for anxiety and depressive disorders. These internalizing problems, however, whether clinical orsubclinical, share many common features and show high comorbidity rates. We emphasize the importance ofsystematic analysis of comorbid anxiety and depression, including their comorbidity with externalizing problems.This could lead to more valid classification of subtypes of internalizing problems and further an understanding ofthe diverse conditions that constitute internalized distress. We highlight the need to study anxiety and depressionwithin a developmental psychopathology framework, as well as to include both categorical and dimensionalassessments of these problems in the same research designs. This will be essential for understanding the complexinterplay of biological and environmental processes that contribute to the emergence, progression, and ameliorationof internalizing problems over time.

The most common forms of child and adoles- nalizing problems. We provide an historicalcent psychopathology have been categorized overview, selectively review the current stateinto two broad classes: internalizing and ex- of knowledge, consider advances and gaps internalizing problems. Whereas externalizing what is known, and identify new research di-problems are characterized by behaviors that rections.are harmful and disruptive to others, internal- We consider both clinical and subclinicalizing disorders signify a core disturbance in anxiety and depression. Initial theories and re-intropunitive emotions and moods (e.g., sor- search on anxiety and depressive disordersrow, guilt, fear, and worry). In fact, both types proceeded largely along independent tracks.of dysfunction have behavioral and affective Although we follow this precedent for histori-components, as well as characteristic cogni- cal clarity, communalities soon become evi-tive features. There is also substantial co- dent, reflecting in part the high comorbiditymorbidity of internalizing and externalizing

rates for anxiety and mood disorders (Not-disorders. The primary focus here is on inter-

tlemann & Jensen, 1995). Investigation of co-morbid conditions and also their links to ex-

Address correspondence and reprint requests to: Carolyn ternalizing problems will be central toZahn–Waxler, Chief, Section on Developmental Psycho- advances in understanding the origins and de-pathology, Child Psychiatry Branch, Bldg. 15-K, Rm.

velopment of different types of internalizing204-A, NIMH, 9000 Rockville Pike, Bethesda, MD20892. problems.

443

C. Zahn–Waxler, B. Klimes–Dougan, and M. J. Slattery444

We highlight the need to consider anxiety seen in normal and subclinical problems? Orinstead, do different etiologic factors operateand depressive disorders within a develop-

mental psychopathology framework, in order to produce different levels of severity of prob-lems? In what ways might early subsyn-to address a number of core questions. How

and why do these serious emotional distur- dromal forms of internalized distress increasethe later likelihood of diagnosed anxiety orbances emerge over the course of childhood

and adolescence? Are there developmental depressive disorders? Different definitions ofproblems, heterogeneity of measures, varia-precursors of these disorders in adolescents

and adults? How are anxiety and depression tions in samples, and severity of problemsstudied across disciplines have made general-conceptualized during the first 2 decades of

life? What are some of the major biological izations difficult. The current article reflectsboth the tensions and opportunities inherent inand environmental factors that contribute to

their emergence? To their co-occurrence? To attempts to integrate psychiatric and psycho-logical approaches. This integration is one ofcontinuity and change over time? How can

the study of normative biological, develop- the major tasks in the new century.The study of internalizing disorders in chil-mental, and socialization processes advance

understanding of the etiology and develop- dren and adolescents originally was based onapplication of adult models to earlier periodsment of internalizing problems?

Psychiatric diagnoses of anxiety and mood of development. This did not encourage, andsometimes impeded, an understanding of thedisorders are based on discrete classification

systems. A clinical disorder is a distinct en- origins and development of these disorders.However, with the advent of a developmentaltity, construed as a disease; it is either present

or absent, depending upon whether specific psychopathology perspective, there has beenan increase in the use of longitudinal and agediagnostic criteria are met. Disorders have tra-

ditionally been viewed as qualitatively differ- cross-sectional research designs to provide in-formation about adaptive and maladaptiveent from the lesser problems of the “walking

wounded” or “worried well.” In psychology, functioning in childhood and adolescence.This makes it increasingly possible to developdimensional classification systems typically

are used to characterize internalizing prob- explanatory models and treatments of inter-nalizing disorders that are grounded in a firmlems (i.e., there is a gradation or continuum

of severity of disturbance). This approach understanding of the phenomenology of theseproblems in childhood and adolescence.does not yield psychiatric diagnoses, though

scores typically are normed, in an effort todistinguish normal, subclinical, and clinical

Anxiety Disordersproblems. There also tends to be less differen-tiation among subtypes of internalizing prob-

Diagnosis and classificationlems in dimensional than categorical systems.Factor analytic work has provided a rationale The diagnosis and classification of anxiety

disorders in children and adolescents is rela-for combining symptoms of anxiety and de-pressed mood into one scale (Achenbach, tively new. The first Diagnostic and Statisti-

cal Manual of Mental Disorders used to clas-1991). At the same time, this precludes com-parisons of the two most prominent types of sify these problems (DSM-II; American

Psychological Association [APA], 1968) rec-internalizing problems.We consider both categorical and dimen- ognized the existence of two disorders: with-

drawing reaction and overanxious reaction.sional perspectives in this article. The differ-ent approaches have led to a series of ques- The DSM-III (APA, 1980) marked a historic

shift to empirically based, behaviorally de-tions that have just begun to surface. Do riskand protective factors known to influence the scriptive diagnostic criteria. A separate diag-

nostic section on “anxiety disorders of child-development of internalizing disorders alsofunction on a continuum? In other words, do hood and adolescence” included separation

anxiety disorder, overanxious disorder, andlower levels lead to less severe disturbance

Internalizing problems of childhood and adolescence 445

avoidant disorder of childhood or adoles- terized by pervasively excessive worry and isseen most often in older children and adoles-cence. The DSM-IV (APA, 1994) identifies

separation anxiety disorder as the only anxiety cents. Social phobia (i.e., fear and avoidanceof social and performance situations) becomesdisorder unique to childhood. Overanxious

disorder and avoidant disorder now are sub- more common in middle childhood and ado-lescence. Panic disorder is rare in childhoodsumed under generalized anxiety disorder and

social phobia, respectively. There are several but more frequent in adolescence. The emer-gence of panic disorder may be associatedother anxiety disorders in DSM-IV that apply

to both adults and children (e.g., panic disor- with puberty (Hayward, Killen, Hammer,Litt, & Wilson, 1992). Obsessive–compulsiveder, agoraphobia, specific phobia, social pho-

bia, obsessive–compulsive disorder, general- disorder consists of repetitive intrusivethoughts (obsessions) or behaviors (compul-ized anxiety disorder, and posttraumatic stress

disorder). sions). Onset occurs during early and middlechildhood (e.g., Swedo, Rapoport, Leonard,Lenane, & Cheslow, 1989; Riddle, 1998).

Epidemiology

Advancements in identification and diagnosisTheory and research

of anxiety disorders in children have contrib-uted to improved epidemiological studies (and Our contemporary understanding of biologi-

cal, environmental, and developmental factorsvice versa). As recently as the mid-1980s, ina review of the extant research (Orvaschel & in the etiology of anxiety disorders reflects a

preceding era characterized by periods of crit-Weissman, 1986) no data were available re-garding anxiety disorders. A decade later in ical reappraisal and integration. Shifts from

general to specific, singular to integrative, anda comprehensive review (Costello & Angold,1995), prevalence rates of 5.7–17.7% for any conceptual to quantitative can be seen within

and between major orientations of study. Aanxiety disorder in children were reported.Other studies have confirmed similar rates. historical review of representative theories

and research exemplifies some of these transi-Differences in prevalence rates may reflectseveral factors. Differentiation of anxiety tions.symptoms from anxiety disorders has largelydepended upon the presence or absence of Psychoanalytic, psychodynamic, and rela-

tional theories. Freud (1936) attributed anxi-functional impairment and subjective distresscriteria. The inclusion of functional impair- ety to the presence of unconscious infantile

libidinal or aggressive wishes towards paren-ment criteria has been shown to decrease ratesof anxiety disorders. The informant may also tal figures, a conception that lost favor over

time. However, the focus on childhood expe-influence rates of reported cases (e.g., chil-dren often report more anxiety symptoms than riences and the quality of the parent–child re-

lationship in shaping children’s sense of secu-are seen in their parents’ reports).Age-related appearance of specific anxiety rity as well as their anxieties and fears has

remained central to several of the psychody-disorders in children has been well docu-mented (e.g., Costello & Angold, 1995). Sep- namic and relational theories that followed.

The collaboration of a psychoanalyst, Johnaration anxiety disorder, the fear of separationfrom primary caretakers, presents most fre- Bowlby, and a developmental psychologist,

Mary Ainsworth, led to theory-driven re-quently during early and middle childhood.Specific phobias (i.e., fear and avoidance of search on the early formation of anxiety prob-

lems that develop in the context of mother–identifiable objects or situations) have beendescribed in children of all ages. Elevated infant interactions and depend on the nature

of the attachment relationship. Caregiver sen-rates of animal phobias may appear in earlychildhood in comparison to social-related sitivity and consistency contribute to secure

attachment, presumably by heightening the in-phobias in adolescence (Marks & Gelder,1966). Generalized anxiety disorder is charac- fant’s comfort and sense of safety (Ainsworth,


1978; Bowlby, 1973, 1988). Attachment theo- be drawn from early experimental studies,generalizations from naturalistic research arerists proposed a relationship between insecure

attachment (anxious–resistant) and the devel- less straightforward. Parents who “model”anxiety and their children who “reproduce” itopment of anxiety in children. Anxious–resis-

tant attachment is, in fact, associated with in- may also indicate shared genetic susceptibilityeither to anxiety problems per se or to biolog-creased fearfulness and inhibited behaviors in

children (e.g., Cassidy & Berlin, 1994). It also ically based, predisposing characteristics (e.g.,low thresholds for physiological arousal).predicts later anxiety disorders in children and

adolescents (Warren, Huston, Egeland, & The role of cognition in theories aboutanxiety has been emphasized in recent dec-Sroufe, 1997).

The theoretical models and empirical re- ades. Research on anxiety disorders in adultsdescribes a bias toward increased attention tosearch generated by Bowlby and Ainsworth

reflect one of the first efforts to investigate threatening or dangerous situations (e.g.,Beck & Clark, 1997). Research on anxiety inthe etiology of (internalizing) disorders within

a developmental psychopathology framework. children suggests similar cognitive processes.Anxious children have been found to interpretTheir pioneering work led to research not

only on the beneficial effects of sensitive ambiguous information as threatening moreoften than nonanxious children (e.g., Hadwin,caregiving but also on the adverse conse-

quences of negative parenting for children’s Frost, French, & Richards, 1997). Biased at-tention to signals of threat or danger areanxiety. Examples of the latter include paren-

tal restriction and negative feedback (e.g., thought to create cognitive distortions througha process of overactivation. Biased attentionKrohne & Hock, 1991), parental high control

leading to perception of low personal control could occur for a number of reasons. In addi-tion to socialization experiences that sensitize(e.g., Chorpita & Barlow, 1998), and maternal

intrusiveness and overprotectiveness (e.g., children to dangerous, anxiety-provoking con-ditions, temperament may render some chil-Bowen, Vitalo, Kerr, & Pelletier, 1995).dren particularly vigilant and vulnerable tooveractivation.Behavioral and cognitive learning theories.

Pavlov’s classical conditioning model of anxi-ety, first used to study the learning of fear in Biological models

Genetic influence. Twin and adoption stud-animals, soon was extended to research withhumans. Its early application to children was ies support the theory that heritable factors

play some role in the expression of anxietyseen in the case of “Little Albert,” a youngchild who was conditioned to develop a spe- problems and disorders (Kendler, Neale, Kes-

sler, Heath, & Eaves, 1992). There is a famil-cific phobia (Watson & Rayner, 1920). Sev-eral theorists (e.g., Rachman, 1977; Seligman, ial pattern seen in the pathogenesis of child-

hood anxiety disorders. For example, there is1971) challenged the overencompassing char-acteristics of the original behavioral model, an increased prevalence in first-degree rela-

tives of children with anxiety disorder com-noting that some stimuli are more biologicallyprone to become feared objects. Also, several pared with relatives of children with attention-

deficit hyperactivity disorder (ADHD) oradditional learning processes have been iden-tified over time. Anxiety could be learned never psychiatrically ill children (e.g., Last,

Hersen, Kazdin, Orvaschel, & Perrin, 1991).from caregivers or others in the child’s envi-ronment (e.g., through modeling and conta- While twin and family studies provide indi-

rect evidence of heritability, specific geneticgion of anxious, fearful behavior; explanatorystyles that emphasize frightening and danger- mechanisms at the molecular level have not

been identified and environmental influencesous aspects of life; or specific child-rearingand discipline practices likely to induce fear are also likely to be operative.

Temperament. Particular temperamentin children through threats or actual inflictionof harm). While causal inferences about the traits may be early indicators of fearfulness or

anxiety. Behaviorally withdrawn and inhib-environment in the learning of anxiety could


ited behavior when encountering unfamiliar have lower baseline cortisol than controlgroups (see review by Stansbury & Gunnar,persons and situations is one such trait (Ka-

gan, Reznick, Snidman, Gibbons & Johnson, 1994). Youths with clinical levels of anxietyhave shown high cortisol reactivity relative to1988). It is postulated to reflect a lowered

threshold of activity in limbic and hypothala- controls, in response to a social challenge(Granger, Weisz, & Kauneckis, 1994).mic structures and has been associated with

increased sympathetic activity (Kagan, Rez- Neurobiological processes and brain cir-cuitry. Advances in science and technologynick, & Snidman, 1987). Family and twin

studies indicate a relationship between behav- over the past few decades have contributedgreatly to our understanding of the biologicalioral inhibition and increased risk of anxiety

disorders (see review by Turner, Beidel, & substrates of adult anxiety disorders. Studiesindicate the likely involvement of multipleWolf, 1996). Generalized social anxiety at ad-

olescence (but not specific fears, separation neurotransmitters and brain structures. Abnor-malities in the serotonin, noradrenergic, andanxiety, or performance anxiety) can be pre-

dicted from behavioral inhibition in the 2nd GABAergic systems have been implicated(Johnson & Lydiard, 1995; Longo, 1998).year of life, though only for girls, suggesting

the moderating effects of gender (Schwartz, There has been very little research with chil-dren.Snidman, & Kagan, 1999).

Physiological regulatory processes. Re- Gray’s neurophysiological model of anxi-ety focuses on approach and withdrawal pat-search on the psychophysiology of internaliz-

ing (and externalizing) problems has pro- terns (Gray, 1982, 1991). They are part of thefight–flight system that responds to protectduced models wherein both classes of

psychopathology have been associated with the organism. Research on neural regulationsuggests differentiating roles of left and rightdistinct physiological profiles. The focus has

been mainly on the autonomic nervous system anterior frontal lobe brain regions in control-ling approach and withdrawal behaviors (Da-(ANS) and the hypothalamic–pituitary–adre-

nal (HPA) axis systems, both of which are vidson & Fox, 1982; Fox, 1991). The leftfrontal brain region is implicated in approachinvolved in the body’s stress response. Anxi-

ety symptoms and disorders have been associ- behaviors and positive emotions, while theright frontal region is associated with with-ated with high heart rates (e.g., Gerardi,

Keane, Calhoon, & Klauminzer, 1994) and drawal behavior and negative emotions. In-fants observed to be high on motor activitydelayed electrodermal habituation (Birket–

Smith, Hasle, & Jensen, 1993). Children hos- and negative affect have shown greater rightfrontal activation at 9 months of age and morepitalized with separation anxiety disorder

were found to have higher heart rates than inhibited behavior at age 14 months (Calkins,Fox, & Marshall, 1996). In another studyother patients (Rogeness, Cepeda, Macedo, &

Fischer, 1990). (Fox, Rubin, Calkins, Marshall, Coplan,Porges, Long, & Stewart, 1996), increasedThe HPA axis system is important in the

regulation of arousal (Gold, Goodwin, & right frontal EEG activation was observed insocially inhibited 4-year-old children. In con-Chrousos, 1988; Stansbury & Gunner, 1994).

Healthy adaptation (indeed survival) relies on trast, left frontal activation was correlatedwith outgoing behavior. These studies providethe ability to produce increased levels of cor-

tisol under stress and to reduce production additional evidence for biological manifesta-tions of inhibited behavior thought to play aonce stress has abated. However, chronic ex-

posure to stress may predispose individuals to role in the development of anxiety disorders.Functional neuroimaging research alsoanxiety and affective disorders, by causing

long-term overproduction of hormones such provides insights into the neurobiology ofanxiety disorders (Rauch, Savage, Alpert,as cortisol in the HPA system. Children and

adolescents with internalizing problems tend Fischman, & Jenike, 1997). Anatomical braincircuits connecting specific brain regions mayto have higher baseline cortisol, whereas

those with externalizing problems tend to be involved, and disruption of components at


varying points in the circuit may produce sim- where parental influences on children’s emo-tional states have been found (Ge, Best, Con-ilar symptoms. Here too, research has been

based primarily on adult and animal models. ger, & Simons, 1996; Ge, Conger, Lorenz,Shanahan, & Elder, 1995). This may be an-Pine and Grun (1999) review neuroanatomical

models of childhood anxiety correlates of other “critical period” in which to study theinteraction of nature and nurture.adult phobias, generalized anxiety, and panic

disorder. These disorders are postulated to re-flect abnormalities in limbic-based amygdala,

Depressive Disordersseptohippocampal, and brain stem–hypotha-lamic circuits. A potentiated startle reflex via

Diagnosis and classificationenhanced amygdala activation may identifychildren at risk for phobic disorders (Davis, Our focus is on the two most common mood

disorders, major depressive disorder (MDD)1997; Grillon, Dierker, & Merikangas, 1997).Septohippocampal dysfunction is believed to and dysthymic disorder (DD; APA, 1994).

Manic–depressive disorder is rare in child-contribute to generalized anxiety disorder inadults and children (Daleiden & Vasey, hood and adolescence and is not considered

here. There is relatively little systematic data1997). Neurocircuits connecting brain stemperiaquaductal gray and the medial hypothala- available on its phenomenology and rates of

occurrence. This is changing, however, andmus may play a role in the etiology of separa-tion anxiety and panic (Panksepp, 1998; there is now heightened interest in the study

of bipolar disorder within a developmentalShekhar & Keim, 1997). Caution is war-ranted, as little is yet known of the biological framework (Akiskal, 1998; Carlson, Bro-

met, & Sievers, 2000). By the 1970s, similari-development of specific brain circuits andhow this relates to development of anxiety. ties were noted in childhood and adult uni-

polar depression, and they came to beBridging research efforts are needed to fur-ther our understanding of the complex inter- considered isomorphic disorders (e.g., Malm-

quist, 1971). Depression in children and ado-play of biological and environmental factorsthat lead children toward or away from having lescents began to be diagnosed using adult

criteria. Major depression in childhood isanxiety problems. Davidson and Rickman (inpress) report associations between right fron- characterized by a period of disturbance in

mood that may include depressed affect, an-tal brain activation and behavioral inhibition,in a sample of children studied at both 3 and hedonia, or irritability. Cognitive or vegeta-

tive symptoms must also be present. Dysthy-9–10 years of age. Inhibition was stable overtime, only for a small subgroup that also had mic disorder is a persistent, milder, but more

chronically depressed mood (or irritability forshown right frontal asymmetry at both timepoints. In keeping with a diathesis–stress children). Cognitive or vegetative symptoms

also may be present. With few exceptionsmodel, the authors speculate that behavioralinhibition may not remain stable for most (e.g., irritability manifest instead of depressed

mood, duration criteria for DD), DSM-IV cri-children with a biological predisposition, dueto the impact of early training and experience teria for child and adult mood disorders are

nearly identical.on neural plasticity. Many individuals are sat-urated with particular emotional climatesfrom early in life. These different emotional

Epidemiologyenvironments could contribute either to stabil-ity or change in inhibition over time, through Overall the prevalence rate of MDD children

ages 4–18 years is between 2 and 8% (Poz-differential, experiential shaping of the emo-tional circuitry of the brain. While Davidson nanski & Mokros, 1994). Rates are low in

childhood. Less than 1% of preschoolers andand Rickman emphasize the importance ofearly experience, plasticity (and hence shap- about 2% of school-aged children meet crite-

ria for MDD (Kashani & Orvaschel, 1988),ing) is possible at other points in develop-ment. Adolescence is a period of rapid change, but by adolescence the rates are between 2


and 8%. There is an increase in prevalence ternalized processes. It was assumed thatchildren did not have the ego- and cognitive-between ages 15 and 18 years. Adolescents

report lifetime prevalence rates of MDD as developmental capabilities to experience sus-tained guilt, misery, and despair (i.e., thosehigh as 15–20%, comparable to adult rates

(e.g., Lewinsohn, Clarke, Seeley, & Rohde, symptoms of internalized distress that are partof the depressive experience). Later it was1994). The prevalence of DD is less than 2%

in childhood and up to 8% in adolescence proposed that depression in children might be“masked” or manifest as “depressive equiva-(Lewinsohn, Hops, Roberts, Seeley, & An-

drews, 1993). Children whose first affective lents,” seen in somatic complaints or behav-ioral disturbances (e.g., Cytryn & McKnew,episode is DD are about 2 years younger at

time of onset than children whose first epi- 1972; Sperling, 1959). It is now clear thatyoung children are capable of the experiencessode is MDD (Kovacs, Akiskal, Gatsonis, &

Parrone, 1994). implicated in the phenomenology of depres-sion, such as excessive guilt (see review byThere are also age changes in the phenom-

enology of depression. In a comparison of de- Zahn–Waxler & Kochanska, 1990) and otherintropunitive emotions. Spitz and Wolf’spressive symptoms in children and adoles-

cents with MDD (Ryan, Puig–Antich, (1946) seminal work on anaclitic depressionin infants in orphanages indicated the pres-Ambrosini, Robinovitch, Robinson, Nelson,

Iyengar, & Tworney, 1987), many similarities ence of depressive syndromes very early inlife. Acknowledgment that young children arewere found (e.g., severity, depressed mood,

insomnia, irritability, suicidal ideation). How- capable of grief reactions (Bowlby, 1960) alsohelped pave the way for theory and researchever, prepubertal children had more somatic

complaints and psychomotor agitation (as on the development of depression in child-hood.well as separation anxiety and phobias), while

adolescents had more anhedonia, hopeless- Psychodynamic views of family relationsinfluenced later research by developmentalness or helplessness, and hypersomnia. Rela-

tive to adults, adolescents are more often psychologists on parenting practices and fam-ily processes associated with child and adoles-changed by an episode of major depression,

in ways suggesting that early-onset depression cent depression. Based on an attachment per-spective, healthy development was thought tois a more pernicious, severe form of the disor-

der (Rohde, Lewinsohn, & Seeley, 1994). be promoted by a family environment charac-terized both by close relationships and thefostering of autonomy. Low levels of parental

Theory and researchwarmth and support, as well as parental rejec-tion, hostility, and family conflict, are knownPsychoanalytic, psychodynamic, and rela-

tional theories. Beginning with Freud, psy- to be associated with depression in childrenand adolescents (McCauley, Pavidis, & Ken-choanalytic theories have emphasized the im-

portance of unresolved childhood experiences dall, in press). Longitudinal research designsdemonstrate the predictive power of observedthat result in adult depression, in particular

the loss of a real or imagined love object. One parental characteristics such as hostility andlow warmth on adolescents’ depressive symp-common theme is that repeated disappoint-

ments and parental failures to meet the child’s toms over time, controlling for initial symp-toms levels (Ge et al., 1996). Other observa-psychological needs may give rise to depres-

sion. Unconscious reactions to early child- tional research also has identified adverseconditions (i.e., less supportive, more conflic-hood circumstances, which also included sex-

ual and aggressive impulses toward parents, tual family environments associated withgreater depressive symptomatology in adoles-were thought to result over time in harsh su-

perego development, as extreme guilt, high cents, both concurrently and prospectively;Sheeber, Hops, Alpert, Davis, & Andrews,standards, and self-blame became internal-

ized. Adult depression, but not childhood de- 1997). Longitudinal research has tended to fo-cus on samples with low to moderate levelspression, was believed to result from these in-


of depressive symptoms. The impact of the Abramson, 1984). Greater integration of thisliterature with developmental research onenvironment on depressive disorders is un-

known and remains an important topic for in- self-concept and emotion regulation is war-ranted, given the low self-regard and dysregu-vestigation. An increasingly prominent view

attributes youth depression to a combination lated emotions that characterize depression.of psychological stress and biological vulner-ability that impact the individual (i.e., a diath- Biological models.

Genetic influence. Twin and adoption stud-esis-stress model; Post, Weiss, Leverich,George, Frye, & Ketter, 1996). ies in adult populations suggest that genetic

factors account for at least 50% of the vari-ance in the transmission of mood disorders.Behavioral and cognitive learning theories.

Behavioral theories of depression emphasize Although genetic factors may increase risk fordepression, environmental factors, particu-the importance of learning and environmental

contingencies. The initial demonstration of larly nonshared experiences within and out-side the family, including differential treat-“experimental neurosis” in Pavlov’s labora-

tory led to a host of studies using similar para- ment of children by parents (Plomin, 1994)also have an impact. The interaction of ge-digms to create symptoms of anxiety and de-

pression (reviewed by Mineka & Kihlstrom, netic and environmental factors has been hy-pothesized in the development of more severe1978). Overmier and Seligman’s (1967) study

was the first, however, to have specific impli- forms of depression (Rende, Plomin, Reiss, &Hetherington, 1993). Increased prevalence ofcations for depressive symptoms. Dogs ini-

tially exposed to uncontrollable shock became depressive disorder has been observed in rela-tives of depressed youth. Children of a de-impaired in subsequent efforts to escape from

or control shock. The model has been applied pressed parent are at substantial risk for de-pression, and risk increases further if bothto other species (Maier & Seligman, 1976;

Mineka & Henderson, 1985), culminating in parents are affected (Birmaher, Ryan, Wil-liamson, Brent, Kaufman, Dahl, Perel, & Nel-the “learned helplessness” model of depres-

sion where the organism learns to give up in son, 1996; McCauley et al., in press).Physiological regulatory processes. Inchallenging, aversive, stressful situations.

The concept of depression stemming from contrast to research on anxiety, there has beenlittle emphasis on the role of temperament inlearned helplessness was expanded to include

cognitive distortions characterized by certain depression. Physiological processes, however,have been studied and many factors associ-attributional styles in adults (e.g., failure at-

tributed to stable, global, internal factors; Se- ated with anxiety are also part of a depressiveprofile in adults. High resting heart rates andligman, Abramson, Semmel, & von Baeyer,

1979). A crosscutting theme of several cog- low electrodermal activity and reactivity typi-cally have been found for adult depressed pa-nitive–behavioral theories is that repeated,

uncontrollable aversive environmental experi- tients (Lahmeyer & Bellur, 1987; Thorell,Kjellman, & D’Elia, 1987), a pattern reportedences create distortions (e.g., negative sche-

mas, biased attributions, negative self-con- earlier for anxiety. Little research has beendone with depressed children and adolescents.cept) or behavior deficits (e.g., deficient

social skills). Distortions thus can create risk Disturbances in HPA axis function also areassociated with depression. Many adult pa-for or become part of the depressive experi-

ence. While most cognitive–behavioral theo- tients tend to have elevated basal cortisol lev-els, show a flattening of the circadian rhythm,ries originally focused on adult depression,

there have been downward age extensions to and fail to suppress cortisol production in re-sponse to the DST test (Akil, Haskett, Young,childhood and adolescence. Several studies

have shown associations between depression Grunhaus, Kotun, Weinberg, Greden, & Wat-son, 1993). This line of research has been ex-and cognitive style in children that are consis-

tent with adult models (e.g., Seligman, tended to the study of depressed children andadolescents. Evidence of HPA axis dysregula-Peterson, Kaslow, Tanenbaum, Alloy, &


tion has not been observed in children and ad- mothers show reduced left frontal EEG activ-ity (e.g., see Dawson, Frey, Self, Panagio-olescents with the frequency and consistency

seen in studies of depressed adults. Several tides, Hessl, Yamada, & Rinaldi, 1999). Thispattern has been replicated many times, andstudies of baseline plasma cortisol secretion

comparing depressed child and adolescent recent work suggests the role of environmen-tal processes in patterns of brain asymmetryoutpatients with controls revealed no signifi-

cant differences. Some other studies have related to emotionality. Reduced left frontalEEG activity can be predicted from observedfound results similar to those with depressed

adults who fail to show cortisol suppression maternal behaviors toward their infants duringplay even after accounting for maternal de-following the Dexamethasone Suppression

Test (DST; see review by Birmaher et al., pression (Dawson, Frey, Panagiotides, Self,Hessl, & Yamada, 1997). These mothers were1996).

Neurobiological processes and brain cir- less affectionate, less engaged during play,and more intrusive.cuitry. Consistent with research on anxiety

disorders in adults, several neurotransmitters Post et al. (1996) have presented a modelthat places affective illness in the context ofhave been identified in the pathophysiology

of mood disorders, including abnormalities in an evolving developmental neurobiologicalframework and a series of molecular neurobi-the serotonergic, noradrenergic, and GABA-

ergic systems. Information about brain re- ological adaptations. Environmental experi-ences are postulated to mediate effects ongions and circuitry associated with depression

in adults has been derived from accumulated gene expression, including psychosocial stres-sors and the neurobiology of episode recur-research based on brain lesions, neuroimag-

ing, and electroencephalographic (EEG) ac- rence. In this view, social support may be ca-pable of generating an inhibitory effect ontivity. As previously discussed, the left frontal

brain region is associated with approach and illness progression by decreasing the percep-tion and neurobiological impact of stressorspositive emotions; the right frontal lobe is in-

volved in internalizing patterns of withdrawal (even at the level of gene expression).and negative emotions that include sadnessand depressed mood. Studies that investigate

Anxiety and Depression: A Developmentalmood have implicated both frontal and pari-

Psychopathology Perspectiveetal regions of both left and right hemispheres(Davidson, 1994; Heller, 1990). Individuals Developmental psychopathology has been de-

fined as “the study of the origins and coursewith depressed moods show frontal lobeasymmetry, reflected mainly in low activation of individual patterns of behavioral maladap-

tation” (Sroufe & Rutter, 1984, p. 18), withof the left hemisphere relative to controls. De-pression also has been associated with re- an emphasis as well on factors that contribute

to resilience and adaptive functioning (Cic-duced activity in the right parietal region. Re-lations between frontal and parietal lobe chetti, Ganiban, & Barnett, 1991; Cicchetti &

Schneider–Rosen, 1984; Cicchetti & Toth,activity remain to be studied, as do intercon-nections of cortical and limbic systems impli- 1995, 1998). Because many psychological

problems generally do not arise de novo, butcated in the regulation of moods, includingdepression. Neurochemical transmission be- emerge over time from prodromal or subclini-

cal symptoms, a developmental perspectivetween limbic and cortical structures that affectarousal and activation of various brain struc- permits study of the evolution of a disorder.

It is assumed that the organism and the envi-tures may be a crucial link in the cortical–subcortical interaction (Heller, 1990). ronment are mutually and interactively in-

volved in determining developmental course.While research with children and adoles-cents is quite limited, some studies indicate Even with an established history of problems,

the particular form of psychopathology maypatterns of brain activity in children at riskthat parallel findings with depressed adults. still be in formative stages (Newman, Moffitt,

Caspi, Magdol, Silva, & Stanton, 1996). WhatInfants and young children of depressed


factors contribute to stability or change in in- and curious. Within a functionalist frame-work, emotions are viewed as organizing,ternalizing problems over time? To improve-

ment or deterioration in functioning? To shifts adaptive, and having regulatory functions forinternal dynamic processes and interpersonalin types of disorders (e.g., from anxiety to

depression)? To different patterns of comor- interaction (Campos, Barrett, Lamb, Gold-smith, & Stenberg, 1983). No emotion isbidity?

Recent conceptual, methodological, and intrinsically more adaptive or dysfunctionalthan any other emotion. Emotions per se areanalytic advances make it increasingly possi-

ble to incorporate key factors into transac- not viewed as dysfunctional, but negativeemotions often have maladaptive qualities oftional, longitudinal research, designed to test

ways in which nature and nurture interact to high intensity, long duration, and situationalinappropriateness (Watson & Clarke, 1992).affect developmental outcomes. We now

know more about putative biological and en- Among the prominent dysfunctions are dis-connections between the experiential and ex-vironmental factors that confer risk or protec-

tion. However, we lack data that would help pressive components of emotion (Plutchik,1993), as well as regulatory problems (Cole,to distinguish atypical from normative pat-

terns of development. For example, how do Michel, & Teti, 1994). Internalizing problemsnot only involve prolonged, intense expres-frontal lobe activity (EEG) and reactivity to

stress (ANS and HPA axis activity) differ as sions of anxiety and sadness but also effortsto control or suppress negative emotions.a function of age? What constitutes nonnor-

mative reactions at any given age, as well as Young female adults asked to suppress nega-tive emotion show greater physiological reac-across age? Similarly, how do environmental

processes likely to include observational tivity, which may be costly in the long term(Richards & Gross, 1999). There is a need formethods (e.g., affective climate, parental

warmth or rejection, expression of authority, research on processes by which dysregulationand disconnection develop in childhood, andinstructional and explanatory style) differ as a

function of age? We also lack descriptive data how they relate to psychopathology.One of the earliest developmental tasks inon normative and nonnormative aspects of the

experience, expression, and regulation of childhood involves the ability to regulate be-haviors and emotions in an appropriate man-emotion, as well as many aspects of social

and interpersonal development. How do these ner. Most children show varying degrees ofmastery of this process. They are able to copeprocesses differ at a specific point in time, or

across time, including developmental varia- with the challenges in their everyday lives inways that allow them to become increasinglytions that may result from different socializa-

tion experiences? Considerable research effort independent and socially skilled. A number ofchildren show deficits in the first years of life,will need to be devoted to this issue in the

21st century. There are several other issues and may be diagnosed with regulatory disor-ders. Problems in these early years are amor-central to an understanding of the phenome-

nology and etiology of internalizing problems phous and difficult to characterize, comparedwith later development, where there is in-from a developmental perspective that have

not received adequate attention. We consider creased differentiation and specificity. Theways in which very young children’s fearful-them next. They include the roles of emotion,

comorbidity, gender, and culture. ness, anger, and failures to regulate emotionaldistress relate to internalizing (and comorbidexternalizing) problems by late preschool and

Emotions and Internalizing Problemsearly elementary school remains unclear.

Negative emotions become more manage-Emotion regulation and dysregulation

able with time for most children. Nervoussystems mature, children come to understandThe lack of emphasis on analysis of the roles

and functions of emotions in the development the meaning, complexities, and consequencesof their feelings, and they develop copingof anxiety and mood disorders is both notable


strategies. Socialization also is thought to play From a developmental perspective, early af-fective biases that may precede or be part ofa role, including the learning of display rules

(i.e., what to conceal, what to reveal, what are the depressive experience are likely also to in-volve worry and anxiety; guilt, shame, andthe appropriate forms of expression). This lit-

erature, however, is based mainly on age self-reproach; lack of pleasure (anhedonia);suppression of anger and hostility; and em-cross-sectional comparisons of different age

groups. We still know little about individual pathic overarousal where the self becomessubmerged in the problems of others. Recalldifferences in regulatory processes, how at-

risk samples compare with normative groups, that the moral emotions such as guilt werefirst implicated in adult depression by Freud,and how this relates to the development of

specific emotional and behavioral problems. who emphasized childhood precursors of thisdisorder, seen in a harsh superego and inter-We do know that regulatory problems con-

tinue throughout childhood, adolescence, and nalization of criticism and blame. Differentconfigurations of emotional profiles may beadulthood, the implications of which merit

further attention. markers of different subtypes of anxiety anddepression.

Emotions and the developmentof psychopathology Comorbid anxiety and depression

Comorbidity rates for anxiety and depressiveSome emotion theorists have focused on func-tional continuities between emotions as epi- disorders can range as high as 70%, with rates

from 20 through 50% most likely to be re-sodic states and psychopathology (Izard,1977; Malatesta & Wilson, 1988). The repeti- ported (see reviews by Angold, Costello, &

Erkanli, 1999; Brady & Kendall, 1992). In ad-tive nature and the emotional salience of ev-eryday social interactions become the basis olescents, there is actually greater comorbid-

ity between anxiety and depressive disordersfor affective biases. These biases are thoughtto become the central organizing axes for per- than among anxiety disorders, and comorbid-

ity is much more common than the “pure”sonality over time. When they become con-solidated through repetitions of discrete emo- types. Comorbidity rates are likely to be un-

derestimated (e.g., major depression accom-tions, and organized into rigid patterns, thismay lead to specific forms of psychopathol- panied by subclinical anxiety would not qual-

ify as comorbidity). Yet the co-occurringogy. Examples include anger biases or traitsin antisocial personality, sadness in depres- anxiety could have significant clinical impli-

cations later in development. Links betweension, and fear in some anxiety disorders.Models based on these views remain to be depression and anxiety have been construed

in different ways: comorbidity may indicatetested in longitudinal research, focusing bothon child characteristics (e.g., stress reactivity the presence of a single underlying dimen-

sion; separate, distinct disorders; or concep-seen in ANS and HPA arousal) and socializa-tion experiences (e.g., how parents and peers tual and measurement problems signaling the

inability of categorical systems to reliablyrespond to negative emotion displays) thatshape particular affective biases implicated in characterize the relevant phenomena. There is

now increased recognition of ways in whichparticular disorders.Advances in research on emotions and in- the study of comorbidity can inform our un-

derstanding of the development of the differ-ternalizing disorders will require expandedconceptions of the structure and organization ent forms of psychopathology (Angold et al.,

1999).of affects implicated in these problems. Bothanxiety and depressive disorders clearly are Anxiety disorders in childhood and adoles-

cence often precede and predict later depres-characterized by more than one prevailingemotion. For example, while sadness is a cen- sive disorders. Initial evidence was based on

retrospective accounts of lifetime histories ob-tral emotion–trait–bias linked to depression,other emotions are arguably as important. tained from diagnostic interviews. For exam-


ple, in one study of children with comorbid tively rare in childhood. Or it may be thatcontinuity is present but takes a less directanxiety and depression, two thirds became

anxious before they became depressed (Ko- form (i.e., from early anxiety to later depres-sion). Anxiety does show stability over timevacs, Gatsonis, Paulauskas, & Richards, 1989).

Several prospective, longitudinal studies have (e.g., first-grade children’s self-reported anxi-ety symptoms had significant prognosticfound that anxiety temporally precedes de-

pression in children, adolescents, and even value in terms of their anxiety symptoms andadaptive functioning in fifth grade, based onyoung adults (e.g., Breslau, Schultz, & Pe-

terson, 1995; Cole, Peeke, Martin, Truglio, & an epidemiologically defined sample; Ialongo,Edelsohn, Werthamer–Larrson, Crockett, &Seroczynski, 1998; Lewinsohn, Gotlib, &

Seeley, 1995). Also, prepubertal-onset anxiety Kellam, 1995).Because anxiety involves dysregulation ofdisorder precedes later recurrent major de-

pressive disorder across several generations of limbic, vegetative, and autonomic systems,the heightened, sustained arousal eventuallyfamilies at high risk for depression (Warner,

Weissman, Mufson, & Wickramaratne, 1999). taxes these systems in ways that cause the or-ganism to shut down and withdraw from envi-A common theme surfaces across theories,

regarding the causal role anxiety may play in ronmental stimulation—in short, to becomedepressed. Not all forms of depression arethe emergence of some forms of depression.

The precipitating role of anxiety in the devel- preceded by anxiety, and anxiety does not in-variably lead to depression. But the patternopment of depression is consistent with an at-

tachment perspective (Bowlby, 1960): the ini- occurs with sufficient regularity to postulate asubtype of depression that differs in its devel-tial response to object loss consists of anxiety

and agitation, depleting the organism and re- opmental history from depression that has notbeen preceded by anxiety. It is noteworthy,sulting in despair. Over time, the anxiety be-

comes intolerable and the organism gives up, too, that the opposite pattern of depressionleading to later anxiety has not emerged as aresulting in depression. Cognitive theories

postulate causal models in which anxiety has developmental phenomenon.The question of whether anxiety and de-a direct influence on liability for major de-

pression. In the learned helplessness model of pressive disorders are meaningfully distinct orpart of a common constellation has been con-depression, the initial response to an uncon-

trollable situation is to become highly anx- sidered extensively in work on “negative af-fectivity” or “internalizing syndrome” in bothious. One developmentally relevant model fo-

cuses on the role of rumination in the children and adults (e.g., Brady & Kendall,1992; Clark & Watson, 1991; Kendler, Neale,prediction of current and subsequent depres-

sion (Nolen–Hoeksema, 1998; Nolen–Hoek- Kessler, Heath, & Eaves, 1992; King, Ollen-dick, & Gullone, 1991). Overlapping and dis-sema & Girgus, 1994). Rumination is the ten-

dency to focus passively and repetitively on tinct features of anxiety and depression havebeen explained using a tripartite modelone’s symptoms of depression without taking

action to relieve them. It involves worry, per- (Clarke & Watson, 1991). The model postu-lates that anxiety and depression share a gen-severation, and even obsession about one’s in-

ner state. Anxiety and worry have childhood eral distress factor referred to as “negative af-fectivity.” Low levels of positive affectivityorigins; hence, ruminative qualities may

emerge at point in time prior to signs of de- are relatively unique to depression, and so-matic tension and arousal are relativelypression. The ruminative process can feed

upon itself so as to magnify the problems, unique to anxiety. This three-factor model hasbeen challenged by data suggesting other fac-overwhelm the child, and eventually create a

state of depression. Unlike disruptive behav- tor solutions (Burns & Eidelson, 1998) andvariations in factor solutions for children as aior problems, depression does not show a

great deal of stability from childhood to ado- function of age (Cole, Truglio, & Peeke,1997). However, it provides an importantlescence. It may be a discontinuous phenome-

non, reflecting the fact that depression is rela- starting point for further research on the phe-


nomenology of internalizing problems, by and externalizing problems clearly emerge asseparate factors, they are also significantly in-focusing on different affective cores that un-

derlie different types and combinations of in- tercorrelated, again indicating their often co-morbid nature.ternalizing problems.

Anxiety and depression also have been as- There is growing evidence that diverseconstellations of behavior may reflect diversesociated with different forms of cognitive pro-

cessing (see review by Mineka, Watson, & etiologies, having different correlates and de-velopmental pathways. For example, Harring-Clark, 1998). An attentional bias for threaten-

ing information is primarily associated with ton, Fudge, Rutter, Pickles, and Hill (1990)found that children with depressive disorderanxiety, memory biases are primarily associ-

ated with depression, and judgmental or inter- were 4 times more likely to suffer from somedepressive disorder in adulthood. However,pretive biases are associated with both anxiety

and depression. This is consistent with Oatley the children with depression and conduct dis-order had lower rates of depression in adult-and Johnson–Laird’s (1987) proposal that

there may be unique modes of cognitive oper- hood than did children with pure depression.The presence of anxiety in antisocial youth,ation associated with different basic emotions.

In this view, depression and anxiety evolved assessed in terms of autonomic reactivity, alsoappears to reduce later criminal behaviorin response to different environmental cir-

cumstances. Anxiety, like fear, is associated (e.g., Raine, Venables, & Williams, 1995).Depression or anxiety may function as a pro-with scanning the environment in anticipation

of potential threat. Depression involves reflec- tective factor, reducing conduct problemsover time. Children with conduct disordertive consideration of events that have led to

failure and loss. Research on childhood ante- also have shown higher levels of cortisolwhen a comorbid anxiety disorder was pres-cedents of different biases is warranted

(Zahn–Waxler, 2000). ent (McBurnett, Lahey, Frick, Risch, Loeber,Hart, Christ, & Hanson, 1991), providing cor-roborative neuroendocrinological evidence for

Comorbid internalizing andthe anxiety component. Other research has

externalizing problemsfound the opposite pattern. For example, thelink between aggression early and late in theThe incidence of disruptive behavior disor-

ders (conduct, oppositional, ADHD) is ele- school year in first-grade males was strength-ened by the presence of comorbid anxiousvated in youth with either mood or anxiety

disorders (see reviews by Compas & Ham- symptoms, rather than attenuated (Ialongo,Edelsohn, Werthamer–Larrson, Crockett, &men, 1994; Nottelmann & Jensen, 1995).

There is also substantial comorbidity between Kellam, 1996). Considerable conceptual andempirical work is needed to unravel the com-internalizing and externalizing syndromes,

seen in Achenbach scores in the .50s and .60s plex and diverse ways in which having onetype of problem influences the developmental(e.g., Hinden, Compas, Howell, & Achen-

bach, 1997). The common and distinct fea- course of another comorbid condition.Calculations of comorbidity rates for inter-tures of internalizing and externalizing prob-

lems have been studied in a birth cohort at nalizing and externalizing problems are basedon the research sample as a whole. While sub-ages 18 and 21 years (Krueger, Caspi, Mof-

fitt, & Silva, 1998). Latent structure and sta- samples can be identified based on differentconstellations of overlapping disorders, therebility of 10 common DSM-III-R (APA, 1987)

mental disorders were examined. A two-factor have been few efforts to develop distinctiveprofiles based on these subgroups. Such anmodel in which some disorders reflected in-

ternalizing problems and others reflected ex- approach would permit greater in-depth anal-ysis of possible different etiologies. Both cat-ternalizing problems provided the most opti-

mal fit to the data. Individuals retained their egorical and dimensional approaches could beused in concert to identify and investigaterelative positions to a significant degree, over

the 3-year period. Even though internalizing subtypes of internalizing problems that be-


come lumped together in calculations of co- associated with problems (e.g., anger, fear,sorrow).morbidity. This would facilitate examination

Future research would benefit from longi-of the implications of symptoms versus a di-tudinal research designs that also includeagnosis of depression (Gotlib, Lewinsohn, &variables based on direct assessments of bio-Seeley, 1995). This complementary approachlogical (e.g., DNA, dopaminergic and sero-could help to establish more veridical profilestonergic neurotransmitters) and environmentalfor types of internalizing problems (Klimes–(e.g., specific types of childrearing and disci-Dougan, Kendziora, Zahn–Waxler, Hastings,pline practices) processes. The influence ofPutnam, Fox, Suomi, & Weissbrod, 1997).these factors could then be estimated in mod-Detailed analysis of different constellations ofels based on direct assessments of these fac-symptoms within a diagnostic category couldtors rather than on inferences derived solelyhelp further to refine the classification pro-from the degree of genetic relatedness. Withcess.regard to environmental processes, other lon-A number of broad classes of dysfunction,gitudinal research on the co-occurrence of ad-expected to create a range of adverse environ-olescent depressive symptoms and conductmental conditions for children, have been as-problems in adolescents has measured parent-sociated with both internalizing and external-ing effects directly (Ge et al., 1996). Differentizing problems (e.g., Gotlib & Avison,observed parenting behaviors predicted both1993)—for example, psychosocial stress,the separate occurrence and the co-occurrencepoverty, parental marital discord, parentalof these internalizing and externalizing prob-psychopathology, maltreatment, and parentallems at later time points, controlling on initialemotional unavailability. A concentration ofproblems. Research that incorporates themultiple risk factors is typically found instrengths of both types of designs (i.e., geneti-more severe and varied problems in childrencally informed samples and actual measure-(Sameroff, Seifer, & Bartko, 1997). Selectionment of environmental, and biological, vari-of well-defined samples will be important forables) will be central to scientific advances inidentifying environmental factors specific tothis area.the development of internalizing, externaliz-

Finally, we consider the implications ofing, and comorbid problems.

comorbidity of emotions for understandingDepressive symptoms and antisocial be-

the phenomenology of internalizing problems.havior appear to share a common genetic

Basic or discrete negative emotions such asdiathesis. They may co-occur because of a fear, sadness, and anger co-occur as blends incommon genetic liability that increases vul- normal individuals (e.g., Watson & Clark,nerability to both types of problems (O’Con- 1992) and in those with clinical conditionsner, McGuire, Reiss, Hetherington, & Plomin, (Biederman, Farone, Mick, & Lelon, 1995;1998). In this work, genetic influences were Kovacs, Feinberg, Crouse–Novak, Paulaus-identified separately for depressive symptoms kas, & Finkelstein, 1984). Terms such as “sul-and antisocial behavior, and for their co-oc- len,” “moody,” or “irritable” are used to de-currence, in adolescents studied using a twin- scribe emotional states that become moresibling design. O’Conner et al. (1998) hypoth- traitlike blends of different negative emotionsesize that depressive and antisocial symptoms seen in both internalizing and externalizingmay be correlated because genes influence a problems. Future research could focus on pro-neurotransmitter system associated with both cesses by which certain emotions within thebehavioral syndromes. Such a view would be comorbid constellation come to predominateconsistent with the demonstrated efficacy of (e.g., the child who initially is both angry andsome psychopharmacological agents in treat- fearful, but who eventually is characterizeding both internalizing and externalizing syn- primarily by fearfulness). Negative emotionsdromes. The medications may help to regulate thus could become differentially channeledemotionality and, hence, act more generally (e.g., as one comes to predominate over time

to influence the ultimate form of disorder).upon the wide a range of negative emotions


Symptoms of irritability, in particular, twice as likely (sometimes more) as males tobecome anxious and depressed, a pattern thatcharacterize both internalizing and externaliz-

ing disorders. Features of major depression continues throughout adulthood. Comorbidityof anxiety and depressive disorders is muchamong clinically referred children and adoles-

cents include a high frequency of dysphoria more common in girls than boys (Lewinsohn,Rohde, & Seeley, 1995); moreover, havingand irritable or angry mood (Biederman et al.,

1995; Kovacs et al., 1984). Irritability in de- more than one anxiety disorder during child-hood or adolescence is virtually exclusive topressed children is commonly described by

parents and teachers, and is often what leads females (Lewinsohn, Zinbarg, Seeley, Lewin-sohn, & Sack, 1997).to a diagnosis of depression (Poznanski,

1982). And it is not uncommon for anxious Until recently, most of the research onchildhood disorders has focused on external-children to show heightened irritability. This

further underscores the importance of re- izing problems known to be more prevalent inmales throughout the life span, and beginningsearch on the etiology of the dysregulated

emotions central to internalizing disorders. As in early childhood. Because the nature ofproblems more common to girls are also lessnoted, children who meet criteria for major

depressive disorder frequently meet criteria disruptive to others and surface later, researchon etiology and development of internalizingfor ADHD, conduct disorder, and anxiety dis-

orders (Biederman et al., 1995). These rela- problems has lagged. The presence of thisvery strong sex difference, suggests the needtionships would be consistent either with pro-

cesses whereby depression reflects hostile to better understand both constitutional andenvironmental factors that place females atimpulses turned inward or antisocial, disrup-

tive behavior reflects masked depression. Nei- such high risk for anxiety and mood disor-ders. Most explanations have focused on bio-ther process is likely to be completely “suc-

cessful,” hence the manifest comorbidity. logical processes and experiential factorsassociated with adolescence and pubertal de-Affective disturbances associated with disrup-

tive behavior disorders and depressive disor- velopment (see Zahn–Waxler, 2000). Herewe emphasize the significance of processesders thus are not as distinctly different as they

might first appear to be (Cole & Zahn–Wax- set in motion much earlier in developmentthat are more difficult to detect.ler, 1992). Careful analysis of patterns of

emotion dysregulation associated with inter-nalizing and externalizing problems might Dispositional characteristics. Early constitu-

tional advantages for girls may provide ahelp to elucidate their common and separatepathways. This will require research designs number of qualities that decrease risk for

early behavior problems. Young girls, on av-that incorporate genetic, psychiatric, and de-velopmental research designs. The resources erage, show greater language skills, more

rapid physical maturation, and advanced regu-and cooperation necessary make this a daunt-ing task. latory capabilities. This may contribute to

their known advantage in terms of frustrationtolerance, ego and impulse control, internal-

Genderized standards of conduct, empathic sensitiv-ity and ability to interpret others’ emotions,During childhood girls exhibit far fewer exter-

nalizing problems (and less overall psychosocial maturity, and responsible interpersonalbehavior (Zahn–Waxler, 2000). Why then dopathology) than boys, with no clear sex differ-

ences evident in depressive and anxiety girls, who appear resilient and relatively im-pervious to childhood mental disorders, laterdisorders. By adolescence, girls (but not boys)

show a marked increase in anxiety and mood show so many internalizing problems? Conti-nuities may present but in a more subtle form.disorders and symptoms (Lewinson et al.,

1993; Nolen–Hoeksema & Girgus, 1994). Fe- Qualities that protect against antisocial behav-ior could also create risk for internalizingmale sex becomes the strongest risk factor for

internalizing problems. Females are at least problems.


We indicated earlier that anxiety could of- minate more than males, and rumination pre-dicts future depression (Nolen–Hoeksema &ten be a precursor of depression, beginning

in childhood. Girls are more prone to early Girgus, 1994). We propose that risk for someforms of later depression begin in childhood,fearfulness and worry than boys (Silverman,

LaGreca, & Wasserstein, 1995), even norma- more often for girls because of their height-ened reactivity and ruminative styles.tively, and they are somewhat more likely to

be shy and inhibited. Dienstbier (1984) hasproposed that different temperaments might Socialization experiences. The socialization

data reviewed here is quite recent in originlead to different emotion-attributional stylesand levels of guilt. Proneness to emotional and often based on middle-class samples. Dif-

ferential treatment of boys and girls may cre-tension should result in intense discomfortand distress following transgression. When ate conditions that predispose females more

often than males to anxiety and depression.distress is internal, the child is more likely toexperience the links between tension and Girls are more likely than boys to be social-

ized in ways that interfere with self-actualiza-transgression, and come to experience anti-cipatory anxiety. Temperamentally anxious tion (i.e., to be dependent, compliant, and un-

assertive; Hops, 1995). A number of differentchildren may develop “affective maps” oftheir experiences where threat or stress-re- experiences are likely to create greater risk for

females than males (reviewed in Zahn–Wax-lated information becomes particularly salient(Derryberry & Reed, 1994). Similarly, Da- ler, 2000). On average, sons are more valued

than daughters. Even when there is seriousmasio, Tranel, and Damasio (1991) refer to anautomatic guiding system that activates “so- conflict between parents, these couples show

more mutual investment in their sons thanmatic markers” associated with one’s past ex-perience. These “maps” or “somatic markers” daughters. Socialization practices (particu-

larly in fathers) that encourage sex-stereo-may facilitate the early, rapid development ofmechanisms related to conscience, such as typed activities could lead to greater submis-

siveness and dependency on the opinions ofguilt and restraint.Because anxiety is more common in girls others in girls. Parents more often discourage

exploration of the physical environment inthan boys in childhood, and because it is asso-ciated with autonomic arousal (elevated heart girls than boys. And they more often place

pressure on girls to anticipate the conse-rate and electrodermal activity), girls may be-come more physiologically aroused than boys quences of their negative acts. Girls are more

likely to be reinforced for shyness and depen-under particular conditions of interpersonalconflict and distress (Zahn–Waxler, Cole, dency, their successes more often overlooked,

and their physical aggression deemed moreWelsh, & Fox, 1995). Girls may more readilydevelop somatic markers that facilitate inter- serious than for boys.

Parents often have higher expectations fornalization of norms and standards of conduct.This proneness to experience internalized dis- mature interpersonal behavior in girls, are less

tolerant of their anger and misbehavior, andtress also may lead to early rumination, creat-ing a constellation of factors that could more likely to override or negate assertive be-

haviors in girls than boys. Many of the social-heighten risk for developing anxiety andmood disorders. Although this is a viable hy- ization practices directed more often toward

girls contain messages that reflect pressures topothesis, it remains to be tested. Because fe-males are known to be more emotionally re- be prosocial, suppress anger, and curtail anti-

social behavior. Suppression of anger, asser-sponsive than males to the problems ofothers, a wider range of interpersonal contexts tion, and other forms of self-expression may

heighten internalized distress. Over time thismay arouse them. Their automated, internalreactions that also include ruminative scripts may result in the indecision, self-criticism,

self-blame, and low self-esteem that becomemay then contribute to entrenched, general-ized patterns that are later seen as anxiety and part of the phenomenology of the depressive

experience. This is one hypothetical exampledepression. Adolescent and adult females ru-


of how disconnection between experience and than boys across cultures (Crijnin et al.,1997). While adult depressive disorders andexpression of emotions (here, anger and hos-

tility) could contribute to the development of syndromes are more prevalent in females thanmales in virtually all cultures, the ratios differinternalizing problems. It is noteworthy that

females and males do not appear to differ in markedly (Kleinman & Cohen, 1997). InChina, for example, female-to-male rates oftheir experiencing of anger and hostility but

rather in their expression and acting out on depression and completed suicides are strik-ingly disproportionate, with suicide describedthese feelings.as a “normative” response for poverty-stricken rural females. This indicates the need

Culture and the development ofto examine cultural characteristics that lead

internalizing problemswomen from some parts of the world, such asChina, to take their lives more often than men,Almost without exception, research consid-

ered here is based on samples of children and whereas in other places such as the UnitedStates the reverse is true.adolescents from the United States. It should

not be assumed that etiology, prevalence, andphenomenology are consistent across cultures.Cultures vary both on some biological dimen- Reflections and Projectionssions and in the kinds of behaviors they value,forbid, and condone. Both may shape the de- It has been illuminating to chart the remark-

able progress made in our understanding andgree and direction of problems in childhood.There are differences in cultural norms re- treatment of early anxiety and depression over

a relatively short period of time. Until quitegarding displays and regulation of emotions,self-expression, and the role of the self in re- recently these disorders were not thought to

be present in children and adolescents. Sincelation to others (Markus & Kitayama, 1991;Han, Leichtman, & Wang, 1998). These vari- then, several internalizing disorders have been

identified, assessed, classified, and treatedations, as well as different culturally definedways of coping with distress, also may help with a variety of psychotherapeutic and phar-

macological approaches. A number of biolog-to determine whether internalizing problemsbecome predominant (McCarty, Weisz, Wani- ical and environmental factors implicated in

the expression of these disorders have beentromanee, Eastman, Suwanlert, Chaiyasit, &Bond, 1999). This is a little-researched area, studied, as well as risk and protective factors

that heighten or diminish the probability thatone that is ripe for inquiry both into the uni-versality and cultural specificity of processes such problems will surface. We have seen an

increase in multivariate, longitudinal designsthat underlie anxiety and depression.Cross-cultural differences exist in the prev- used to more fully explicate the etiology of

the internalizing symptoms and disorders thatalence and patterning of problems. Internaliz-ing problems in children occur more often in so commonly afflict children and adolescents.

Considerable attention has been devoted tosome countries (e.g., Greece, Thailand, PuertoRico), whereas externalizing problems are the development of methods to assess symp-

tomatology and the factors implicated in theirmore common in other countries (e.g., UnitedStates, Germany, Sweden; Crijnin, Achen- expression. But it is just a beginning. As a

field we are still in a very early developmentalbach, & Verhulst, 1997; MacDonald, Tsiantis,Achenbach, Motti–Stefanidi, & Richardson, period with regard to our theoretical and ap-

plied knowledge base. While transactional,1994). While comorbidity of internalizing andexternalizing problems is common across developmental research is commonly recom-

mended, we have not yet fully incorporatedcountries and cultures, the nature of these re-lationships will vary depending upon which this perspective into our study designs. More-

over, we are still some distance from ascer-type of problem is more prevalent in the dif-ferent cultures. taining the most salient constructs and, in

turn, having the requisite armamentarium ofGirls show more internalizing problems


valid measures needed to test transactional of human suffering. To do so requires a pro-found understanding of the nature of childrenmodels.

The fluid nature of many affective and be- and adolescents across the time course. Symp-toms of internalizing problems are known tohavioral symptoms in children and adoles-

cents continues to raise questions about the vary across different periods of development.Historically, the use of top-down models (i.e.,ultimate forms disorders will take over the

course of time. There are indications of pro- studying anxiety and depression in adults andthen working backward to understand similargression from comorbidity to specificity,

where comorbidity is seen as an earlier devel- problems in children and adolescents) createdproblems that continue to the present day. Inopmental phenomenon (Nottlemann & Jen-

sen, 1995). Initially, psychopathology is psychiatric research, participants who varywidely in age (e.g., from 6 to 16 years) oftenamorphous in form of expression, becoming

more differentiated and clearly defined as per- are considered as one group for analytic pur-poses. This can limit generalizations and,sonalities begin to crystallize and the central

nervous system reaches maturity, especially hence, the utility of the research findings. Itis difficult to develop valid assessment sys-after puberty and midadolescence. For exam-

ple, while current lifetime histories of depres- tems and programs for effective prevention,intervention, and treatment in a nondevelop-sion in adolescents are highly comorbid with

other disorders, the rates are substantially mental context. Psychotherapeutic and phar-macological approaches to treatment alsolower in adults (Rohde, Lewinson, & Seeley,

1991). Adolescent-onset depression may rep- originated from top-down models. Whilemany treatment approaches are now highlyresent a more serious form of the disorder.

Alternatively, it may initially be more undif- sensitive to developmental level, some arenot. Public attention recently has been drawnferentiated, with greater specificity develop-

ing over time. Longitudinal research would to giving children in the first years of life themedications that had been developed and ap-help to address questions about determinants

of these different developmental pathways. proved for treatment of depressive disordersin adults and attentional problems in school-The literature on resilience is beginning to

identify factors associated with a good out- age children. While developmentally sensitiveresearch has become more common, it oftencome despite being reared under conditions of

risk. We know relatively little about what fac- follows rather than precedes treatment deci-sions.tors are protective with regard to internalizing

disorders as compared with other types of Psychologists have in-depth knowledge ofdevelopmental processes. They also havepsychopathology. Many definitions of resil-

ience center on achievement, social compe- methods that, if used in conjunction withthose developed within a psychiatric tradition,tence, or finely honed interpersonal skills

(Beardslee & Podorefsky, 1988; Luthar & would help to establish an integrated percep-tion of the essential need for both categoricalZigler, 1991). Internalizing problems often

coexist with competencies, and “high” func- and dimensional approaches to assess andclassify internalizing problems. It is importanttioning also can reflect aspects of disorder

(Luthar & Zigler, 1991). Consequently, addi- that both psychiatry and psychology deal witha full range of symptomatology. There is ational methods are needed to assess psycho-

logical health as a protective factor. reluctance to wrestle with questions aboutwhether and when a quantitative differenceThe scope of this article did not include

discussion of assessment and treatment, topics becomes a qualitative difference as well, orabout dynamic processes that move the childthat are less often considered within a devel-

opmental psychopathology framework. Scien- from normative, to subclinical, to clinicalsymptoms (or in the other direction). Psychol-tific knowledge of the origins, development,

and phenomenology of internalizing problems ogists who rely solely on quantitative, dimen-sional measures often do not convey the de-is important in its own right. But ultimately

this work is also in the service of valid assess- gree of psychopathology (or lack thereof) thatis reflected in their findings. Psychiatrists whoment and successful treatment of these forms


rely solely on qualitative, categorical mea- pear as temperamental qualities or personalitycharacteristics. In contrast to the stability ofsures based on diagnostic information often

do not have sufficient appreciation of the sig- externalizing problems across time, there islittle empirical evidence of continuity of de-nificance of subthreshold symptoms. Collabo-

rative work would elucidate the wide range of pression. Lack of continuity may reflect thelack of developmental research on internaliz-significant symptoms.

A related issue concerns the models and ing problems, along with the fact that prodro-mal signs may be less obvious. Even less isstatistical approaches utilized in different dis-

ciplines. It has been common in develop- known about the history of anxiety syndromesacross these developmental periods, and prob-mental research for psychologists to test ex-

planatory models using a variable-centered ably for the same reasons. Even with the in-creased awareness of internalizing disordersapproach, attempting to understand develop-

mental trajectories through analyses of the in children, only a minority receives treat-ment. When children evidence more “pure”group as a whole. Such a process does not

lend itself well to understanding of subtypes forms of anxiety or depression, symptomsmay go unnoticed as they suffer in silence.of anxiety and depression either in “pure” or

comorbid form. It is easy for the individual to When they are accompanying externalizingproblems, the disruptive behaviors may ac-become lost in what has come to be viewed as

a “one-size-fits-all” model. A person-oriented tively divert attention away from the anxietyor depression. Some early expressions of anx-approach that focuses on attempting to define

different clusters of individuals is also essen- iety could even be seen as positive as theymay motivate children to behave in ways val-tial. The contributions of developmental psy-

chology and psychopathology will become ued by adults.In summary, anxiety and depressive disor-more salient to child and adolescent psychia-

try (and vice versa) when the disciplines are ders are common in childhood and adoles-cence. These disorders are still understudiedable to interface more on problems that would

be expected to be of common interest. relative to other disorders, highlighting theneed to focus on biological and psychosocialA developmental psychopathology frame-

work has much to offer for understanding the underpinnings of these illnesses. Longitudinalstudies of the course and outcome of anxietyetiology and development of internalizing

problems. There is evidence from prospective and depressive disorders in childhood and ad-olescence are critical—not only to further ourresearch of continuity between adolescent and

adult depression (Rao, Hammen, & Daley, knowledge of the impact of these disordersduring the earlier stages of human develop-1999). Longitudinal research on links be-

tween childhood depression and adolescent or ment but also to increase our knowledge oftheir emergence in adulthood. The progressadult depression has not been conducted. Not

all depression subsequent to childhood would that has been made and the foundations thathave already been established for achievingbe expected to have very early origins, but

depressed adults often report symptoms dat- future goals should encourage us. We alsoshould be prepared for sweeping changes ining back to childhood. Clinical depression

may emanate eventually from subsyndromal how internalizing problems are viewed andstudied in this century.depressive styles that in childhood may ap-

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