Much evidence exists documenting the comorbidity of anxiety and affective disorders in ... comorbid when there is a high rate of symptom overlap between the ...
Clinical Child and Family Psychology Review, Vol. 1, No. 2, 1998
Comorbidity of Anxiety and Depression in Children and Adolescents: An Integrative Review Laura D. Seligman1 and Thomas H. Ollendick1,2
Much evidence exists documenting the comorbidity of anxiety and affective disorders in youth. Furthermore, comorbidity appears to have serious implications both in terms of severity of impairment and course of disorder. Despite this, little is known about the meaning behind the high rate of co-occurrence of anxiety and depression in children and adolescents. Several conditions exist that may give rise to comorbidity. Specifically, two disorders may be comorbid when there is a high rate of symptom overlap between the disorders, when one underlying construct is split into two separate disorders, when the disorders share common risk or etiological factors, or because one disorder causes or increases the risk of developing the second disorder. The present paper examines each of these explanations as they relate to the comorbidity of anxiety and depression in youth. KEY WORDS: Anxiety; depression; comorbidity.
One result of the division of psychopathology into multiple distinct and "separate" categories or syndromes, and more generally the reliance on the neo-Kraepelinian paradigm (a tradition exemplified by the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders), has been the observation that multiple disorders tend to cooccur within the same individual. This overlap has often been termed comorbidity. Comorbidity may imply either the co-occurrence of two or more disorders in an individual at a given time, or the manifestation of multiple disorders during the lifetime of the individual. Understood in this way, an extensive body of literature documents the high prevalence of comorbidity among childhood disorders in general and between anxiety and depression in children and adolescents in particular. Despite the popular notion that comorbidity may be observed in clinical practice because of the self-selection processes that occur in
clinic-referred samples, evidence suggests that comorbidity between anxiety and affective disorders is a phenomenon that exists in both help-seeking and non-help-seeking samples.
Epidemiological Evidence for the Comorbidity of Anxiety and Depression in Youth A surge in the investigation of the epidemiology of childhood psychopathology lends considerable support to the existence of comorbidity of affective and anxiety disorders in youth. For example, the Dunedin Multidisciplinary Health and Development Study investigated the prevalence of psychiatric disorders in a cohort of children born between April 1, 1971 and March 31, 1972, in Dunedin, New Zealand (Anderson, Williams, McGee, & Silva, 1987; McGee et al., 1990). Anderson et al. (1987) examined a subsample of these children at age 11. Specifically, they interviewed 785 children using a structured diagnostic interview and obtained questionnaire data from parents and teachers. Of the 59 children diagnosed with an anxiety disorder, 10 (17%) evidenced a comorbid affective condition. Moreover, 10 of the 14
1
Virginia Polytechnic Institute and State University, Blacksburg, Virginia 24061. 2 Address all correspondence to Thomas H. Ollendick, Virginia Tech Child Study Center, 3110 Prices Fork Road, Blacksburg, Virginia 24061-0355.
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126 children diagnosed with depression/dysthymia were diagnosed with a comorbid anxiety disorder (71%). The prevalence of psychiatric disorder in the Dunedin sample was estimated again when the youth were 15 years of age (McGee et al., 1990). Prevalence estimates were based on a subsample of 943 adolescents who were interviewed using the same structured diagnostic interview. Parents provided additional questionnaire data. A total of 101 of the youth had an anxiety diagnosis at age 15; of these 13 (13%) had a comorbid affective condition. Of the 40 adolescents diagnosed with an affective condition at age 15, 13 (approximately 33%) were comorbid with an anxiety disorder. Thus, in both waves of the Dunedin investigation anxiety and depression were found to co-occur; however, while the rate of depression in children/adolescents who were anxious remained relatively stable, the rate of anxiety in children/adolescents who were depressed decreased dramatically (i.e., from 71 to 33%). One reason may be the methodological differences in determining diagnoses at age 11 and age 15. That is, at age 15 the adolescents were the primary informant and parental data were used to confirm diagnosis; however, at age 11 diagnoses were made using varying combinations of parent, teacher, and child data. In a similar investigation, Kashani and his colleagues estimated the prevalence of DSM-III (American Psychiatric Association [APA], 1980) psychiatric disorders in a sample of 150 adolescents between 14 and 16 years of age enrolled in a public school system in Columbia, MO (Kashani et al., 1987; Kashani & Orvaschel, 1988). Approximately 17% of the sample met criteria for an anxiety disorder based solely on a diagnostic interview conducted with the adolescents; however, only 8.7% (13 of the 150 adolescents) met criteria for "caseness", defined in terms of severity and need for treatment (Kashani et al., 1987; Kashani & Orvaschel, 1988). Of the 13 anxiety-disordered cases, 9 (69%) met criteria for an affective disorder. Although comorbidity of other disorders (e.g., conduct disorder) with anxiety was observed, depression was the most frequent comorbid diagnosis. Similarly, 12 (8%) of the adolescents met criteria for caseness of affective disorder. Of these cases, 9 (75%) were comorbid with an anxiety disorder. Given the very high rates of comorbidity of anxiety and depression in this study (compared to those of the Dunedin group), it should be noted that comorbidity was determined for cases by Kashani and colleagues and simply meeting structured diagnostic
Seligman and Ollendick criteria for an anxiety disorder or affective disorder by Anderson and colleagues. Estimating prevalence of psychiatric disorders in a birth cohort of approximately 1,000 adolescents enrolled in the Christchurch Health and Development Study (New Zealand), Fergusson, Horwood, and Lynskey (1993) found the odds ratio between anxiety and affective disorders was between 4.6 and 4.9 (significantly different than zero). For those with an anxiety disorder, the odds of having a comorbid affective disorder were greater than the odds of having any of the other disorders under investigation, although not significantly so. In summary, substantial evidence exists to document the comorbidity of anxiety and depression in general community samples. However, estimates vary greatly depending upon age of the sample and method for determining diagnosis.
Evidence for Comorbidity of Anxiety and Depression in Youth in Help-Seeking Samples Clinical samples of children and adolescents often present with comorbid cases of anxiety and affective disorders. This is true regardless of the presenting complaint. For example, turning first to clinical samples presenting for an anxiety disorder, Strauss, Last, Hersen, and Kazdin (1988) examined a sample of 140 youth between the ages of 5 and 17 years seen at a child and adolescent anxiety disorders clinic. Of these children and adolescents, 106 met DSM-III criteria for an anxiety disorder. Approximately 28% of the youth diagnosed with an anxiety disorder were also diagnosed with comorbid major depressive disorder (MDD). Drawing from a sample from the same clinic, Last, Strauss, and Francis (1987) found 15% of their sample to have a primary diagnosis of MDD. Of these youth, all exhibited at least one comorbid anxiety disorder. Studying a clinical sample of depressed children from a psychiatric clinic and a general medical clinic, Kovacs, Gatsonis, Paulauskas, and Richards (1989) reported that 41% of their sample evidenced a comorbid anxiety disorder. Further, an additional 3% were found to be experiencing an anxiety disorder during follow-up interviews. Similarly, Mitchell, McCauley, Burke, and Moss (1988) reported that 43% of the depressed children and adolescents they interviewed when referred for psychiatric inpatient/outpatient treatment had an additional diagnosis
Anxiety and Depression of separation anxiety disorder (SAD). Generalized anxiety disorder (GAD) was also found in 13% of the sample and phobias in approximately 16%.
Implications of Comorbidity Clearly, comorbid presentations of anxiety and affective disorders are common. However, the meaning and implications of comorbidity go beyond its utility as a purely descriptive phenomenon. For example, children with comorbid anxiety and depression are typically more severely impaired than children with either disorder alone (Nottleman & Jensen, 1994). Additionally, comorbidity may have implications for the course of psychopathology. In a sample of adolescents in the Dunedin investigation anxiety comorbid with depression at age 15 was associated with one of the highest rates of any disorder at age 18 (Feehan, McGee, & Williams, 1993). Thus, although comorbidity appears to have a significant impact on disordered individuals, conceptual and practical implications of its presence have been largely ignored. In treatment outcome studies, comorbid conditions often serve to exclude individuals from entry. As such, we know that these individuals represent more severely impaired and disordered populations but we know little about how our treatments impact upon them. More importantly, perhaps, little is known about the pathways to comorbidity or, in other words, the conditions under which comorbidity occurs or why it occurs with such frequency. Surprisingly, little effort has been put forth to explicate the meaning behind the high comorbidity of anxiety and affective disorders in youth. As Rutter (1994) acknowledged: the observation of comorbidity or co-occurrence has to be regarded as a starting point from which to undertake research to investigate the mechanisms that might be involved. It does not in any way provide an explanation of the processes and, for this reason, it can only be regarded as a stimulus to further investigative work. (p. 101)
In this vein, four principal explanations for high rates of comorbidity can be deduced from the literature (Frances, Widiger, & Fyer, 1990). First, although two disorders such as anxiety and depression may be indicative of two distinct underlying constructs, the extent of overlapping definitional criteria may produce high rates of comorbidity. Second, it may be that comorbidity is caused by the splitting of a unitary latent construct into two (or more) categories. Third, two
127 disorders can be comorbid because they share some underlying causal or risk factors. Last, one disorder may cause or put an individual at increased risk for a second disorder. Thus, these first two explanations suggest that comorbidity of anxiety and depression is an artifact caused by the way in which the disorders are defined, whereas the last two explanations suggest that comorbidity is due to the nature of the disorders (e.g., etiology and associated outcomes). The purpose of the present paper is to explore the plausibility of each of these explanations as they relate specifically to the exegesis of the relationship between anxiety and depression in youth. Although an exhaustive review was not undertaken, examples were chosen to be representative of the literature pertaining to each hypothesis.
ANXIETY AND DEPRESSION: SIMILARITIES IN DEFINITIONS? As noted above, the first explanation to be discussed, that overlapping definitions produce the illusion of comorbidity, suggests that comorbidity is an artifact. That is, such a proposition suggests that it is not that "true" anxiety and depression are actually comorbid at greater than chance levels but that they appear to be so because of the ways in which they have been defined and identified via our diagnostic systems. For such an explanation to be true a number of necessary conditions must be met. First, given the oft-reported finding that children who are depressed are more likely to evidence a comorbid anxiety disorder than the reverse (e.g., Anderson et al., 1987), a higher proportion of anxiety symptoms should be evident in the criteria for depression than the reverse. Second, the degree of comorbidity between diagnostic categories should be directly related to the number of definitional criteria specific diagnoses share. Third, co-occurrence should be dependent upon the presence of overlapping definitions and the significant correlation observed between anxiety and depression should no longer be found when the constructs are defined in unique ways and without significant overlap. A summary of these conditions can be found in Table I. First examining the overlap at the level of diagnosis, examination of extant criteria reveals that, to differing degrees, the anxiety disorders and MDD are defined using similar criteria. While there is no definitional overlap between symptoms of SAD or Social Phobia (SP) and MDD as defined
128 Table I. Criteria for Accepting the Hypothesis that Comorbidity Between Anxiety and Depression in Youth is Due to the Overlap in Definitions 1. Given that the conditional probability of being anxious given the presence of depression is higher than the conditional probability of being depressed given the presence of anxiety, a higher proportion of criteria for anxiety disorders should overlap with depression than the reverse. 2. Rates of comorbidity between specific anxiety disorders and depression should be directly related to the number of definitional criteria which they share. 3. Correlations between assessment instruments measuring anxiety and assessment instruments measuring depression should no longer be significant when overlapping items are removed.
by DSM-III-R3 (APA, 1987), 5 of the 19 (26.3%) symptoms of GAD overlap with the symptoms of a major depressive episode. Similarly, of the 9 symptoms of MOD, 5 (55.6%) overlap with symptoms of GAD. This is the reverse of what would be expected based on the hypothesis that symptom overlap accounts for the pattern of comorbidity observed between anxiety and depression. Moreover, to diagnose MDD, either depressed mood or "irritability" in children and adolescents or loss of interest must be present. The symptom of irritability is common to both GAD and depression. However, the symptom that must be present to diagnose GAD (i.e., "unrealistic and excessive worry") does not overlap with symptoms for MDD. Although it is possible that a child or adolescent could meet diagnostic criteria for a major depressive episode based solely on the presence of the same symptoms that would merit a diagnosis of GAD, the reverse is not true. Thus, while symptom overlap alone could explain the presence of MDD in children with GAD, symptom overlap alone cannot explain the presence of GAD in children with MDD, although the degree of overlap present can contribute to the probability of comorbidity. Thus, if definitional overlap were the sole explanation for comorbidity, it should be true that the rate of comorbidity, of depression in children with GAD should be higher than the rate of comorbidity with GAD in children who are depressed. However, as noted above, it is more likely for a child who is depressed to be anxious than it is for a child who is anxious to be depressed. Furthermore, the overlap of other 3
DSM-III-R criteria are illustrated because, to date, little information using DSM-IV (APA, 1994) definitions is available.
Seligman and Ollendick disorders such as SAD and SP with MDD do not contribute to this phenomenon inasmuch as there is no symptom overlap between these disorders and MDD. Since there is variability in the degree of symptom overlap between depression and SAD, SP, and GAD, if symptom overlap is the reason for comorbidity, then it should follow that there should be differential rates of comorbidity between these disorders and depression. The differential rates of symptom overlap of GAD, SP, and SAD suggest that comorbidity should be highest between GAD and MDD and present only at chance levels for SAD and MDD and SP and MDD. To make definitive statements about the veracity of this hypothesis, evidence from epidemiological surveys is essential given that the ascertainment biases inherent in clinical samples preclude statements about true estimates of comorbidity. However, a review of existing epidemiological investigations of psychopathology in childhood and adolescence reveals no studies that use current definitions of disorder and provide estimates of comorbidity separately by type of anxiety disorder. As such, it is necessary to turn to investigations of clinical samples, with the understanding of the inherent limitations in doing so. In one investigation examining comorbidity of depression in SAD, overanxious disorder (OAD) (analogous to GAD), and SP, Last et al. (1987) found that 8.3% of children with a primary diagnosis of SAD, 18.2% of children with a primary diagnosis of SP and none of the children with a primary diagnosis of OAD were also diagnosed with MDD. Moreover of those with a primary diagnosis of MDD, 27.3% also had a diagnosis of SAD, 54.5% also had diagnosis of SP and 45.4% also had a diagnosis of OAD. Similarly, Kovacs et al. (1989) found 41% of the youth they studied with MDD to have comorbid SAD, whereas only 13% of the depressed youth also had a diagnosis of OAD. Although there are several limitations in these comparisons (e.g., selected samples, OAD is not defined exactly as GAD), and it should be noted that the comorbidity of anxiety disorders with one another complicates the interpretation of these findings, these observations are not consistent with the conditions outlined above. In other words, there is not reason to conclude from these relationships that symptom overlap alone can account for the comorbidity between anxiety and depression. A separate but related issue is the overlap in items that are used to assess for the presence of anxiety and depression. With the exception of diagnostic interviews, which typically have items that map directly
Anxiety and Depression onto DSM criteria, the most widely used assessments of anxiety and depression measure these constructs using a dimensional approach rather than a categorical approach. Here too, when anxiety and depression are measured in dimensional terms, the two constructs are found to be significantly correlated. For example, King, Ollendick, and Gullone (1991) found correlations of self-reports of anxiety and depression to range from .46 to .70 depending on the nature of the sample (i.e., clinical vs. community sample) and the assessment instruments used to measure anxiety and depression. The Children's Depression Inventory (GDI; Kovacs, 1985), the Revised Children's Manifest Anxiety Scale (RCMAS; Reynolds & Richmond, 1978), and the State-Trait Anxiety Inventory (STAIC; Spielberger, 1973) are among the most widely used instruments to measure anxiety and depression in youth (King et al., 1991). As with diagnostic overlap, the item overlap of the anxiety scales with the CDI is somewhat variable. Specifically, the CDI and RCMAS have six similar items (22.2% of the CDI and 21.4% of the RCMAS), the CDI and STAIC-State have two similar items (7% of the CDI and 10% of the STAIC-State scale), and the CDI and the STAIC-Trait Scale have five similar items (18.5% of the CDI and 25% of the STAIC-Trait scale). Cole, Thiglio, and Peeke (1997) found that eliminating overlapping items from parent, teacher, peer, and self reports of anxiety and depression decreased the shared variance between the anxiety and depression constructs by approximately 12-14%; however, even with the deletion of overlapping items the constructs continued to be significantly related.
Summary and Conclusions The empirical evidence is not supportive of the conclusion that symptom overlap alone can account for the comorbidity of anxiety and depression in youth. That is, data on symptom overlap are not consistent with the fact that anxiety is more common in those individuals who are depressed than the reverse, nor are rates of comorbidity for specific anxiety disorders directly related to number of symptoms they share with MDD. Moreover, when examining anxiety and depression dimensionally, using self-report instruments, significant correlations exist even when symptom overlap is systematically eliminated. It should be noted, however, that conclusions reached here must be tentative given the limitations discussed above regarding the current state of this literature. First, accurate estimates of comorbidity could not be obtained
129 from epidemiological data because these studies reported comorbidity rates collapsed across all anxiety disorders and not separately. Furthermore, much of the data are based on relatively small samples. Additionally, data on GAD in youth are scarce given that it was just recently decided to eliminate OAD and to merge it with GAD. Thus, data presented for GAD using OAD analogously must be considered with caution. However, Kendall and Warman (1996) have recently demonstrated significant overlap in these disorders, suggesting the probable relevance of these findings. Finally, to answer the questions posed here, future investigations will need to employ large samples and the most current diagnostic definitions in unselected samples so that different anxiety diagnoses can be considered separately. Despite the fact that symptom overlap alone does not appear to provide a good explanation for high rates of comorbidity between anxiety and depression, a good deal of repetition exists in the definitions of anxiety and depression. Given that symptom overlap can result in a situation in which meeting criteria for one disorder can result in partial or complete (as with GAD and a major depressive episode) presence of another disorder, it is necessary to further investigate the degree to which this condition accounts for comorbidity between anxiety and depression in youth. Recent developments in structured/semistructured interviews that allow for investigation at the symptom level make it possible for such hypotheses to be explored; however, to date no studies have analyzed the relationship between anxiety and depression in this manner. Furthermore, data of this type could be used to determine which specific symptoms of anxiety and depression are the most relevant in terms of discriminating between the two syndromes and predicting the negative sequelae of anxiety and depression (i.e., suicide, social neglect). Such evidence could be used to develop a weighting system for diagnostic criteria. However, it must be remembered that symptoms can be signs of more than one disorder; therefore, some degree of overlapping symptomatology is probably to be expected in order to fully define the anxiety and affective disorders.
ANXIETY AND DEPRESSION: BINARY, UNITARY OR OVERLAPPING CONSTRUCTS? Several reviews (e.g., Brady & Kendall, 1992; Stavrakaki & Ellis, 1989) have addressed the issue of whether anxiety and depression are indicators of the
130 Table II. Criteria for Accepting the Hypothesis that Comorbidity Between Anxiety and Depression in Youth is Due to the Fact that Anxiety and Depression Represent Two Indicators of a Single Construct 1. Repeated investigations using exploratory factor analyses should consistently find support for the superiority of the one-factor model over the two-factor model, -and/or2. Repeated investigations using confirmatory factor analyses, should consistently find support for the superiority of the one-factor model over the two-factor model. 3. Investigations should use a variety of samples (i.e., clinical and community samples, boys and girls, different age groups) and adequate sample sizes.
same or distinct constructs. Although these reviews have considered clinical correlates, symptoms, genetic and biological markers, response to treatment, and family history data, no definitive conclusions have been offered. In fact, the plausibility of several interpretations of the data lead to widely disparate conclusions based on the same information. Factor analytic techniques, data reduction procedures in which many indicators can be reduced to a fewer number of factors, theoretically representing underlying latent constructs, provide one direct test of the question of whether anxiety and depression can be best described as one or two latent constructs. Additionally, recent advances in factor analytic techniques have led to confirmatory factor analytic procedures that allow for direct tests of this type of question without the arbitrary assumptions assumed by exploratory factor anlayses. Therefore, to demonstrate the validity of the unitary construct hypothesis for explaining comorbidity between anxiety and depression, it should be found that repeated investigations using exploratory and confirmatory factor analyses which employ a variety of samples and adequate sample sizes provide support for the superiority of one-factor over two-factor models. (A summary of these conditions can be found in Table II.) However, relatively few investigations of childhood anxiety and depression have employed such techniques. Williams, McGee, Anderson, and Silva (1989) conducted one such study utilizing exploratory factor analyses. Williams et al. interviewed at total of 748 children from the Dunedin Multidisciplinary Health and Development Study at 11 years of age. The interviews were conducted as part of the ongoing epidemiological investigation described earlier. Children were interviewed using the DISC (Costello, Edelbrock, Kalas, Kessler, & Klaric 1982) which con-
Seligman and Ollendick tains 13 subscales. Subscale scores were subjected to exploratory factor analyses separately for boys and girls. Results revealed a two-factor structure for boys, one factor representing externalizing symptomatology and the second representing internalizing symptomatology. For girls, a three-factor solution was determined, one factor representing the externalizing symptomatology similar to that found for the boys, a second factor on which all the anxiety scales loaded, and a third factor representing depressive symptomatology. However, for both boys and girls the anxiety and depression factors (boys' scores were computed using the three-factor structure found for girls) were highly correlated, .63 and .55, respectively. In a similar investigation Ollendick, Yule, and Oilier (1991) administered the Fear Survey Schedule for Children-Revised (FSSC-R; Ollendick, 1983), the RCMAS (Reynolds & Richmond, 1978) and the GDI (Kovacs, 1985) to a sample of 9- to 11-year-old British primary school children. An exploratory factor analysis of items from all of the instruments was performed. While factors related to items of the FSSC-R and the lie scales from the RCMAS were relatively uncontaminated by items from the two other measures, two factors were a blend of items from both the GDI and the RCMAS. One factor primarily reflected depression and agitation, whereas the second primarily related to worry, concentration difficulties, and oversensitivity. Additionally, yet another factor reported by Ollendick et al. (1991) consisted of items only from the CDI. Therefore, these studies suggest not only some distinctiveness in anxiety and depressive symptomatology but also a great deal of overlap. In one investigation that directly tested and compared a one- and two-factor model for anxiety and depression in children, Crowley and Emerson (1996) used confirmatory factor analysis to explore the structure of children's self-reported anxiety and depression in a sample of youth between that ages of 8 and 12 years. Results revealed that while the one-factor model did not produce an acceptable fit to the data, the two-factor solution did. Furthermore, comparing the two models, the two-factor model resulted in a significantly better fit. However, examining the adjusted fit index, even the two-factor model did not provide a very good fit with the data. The authors suggested the possibility of a three-factor model in which one factor might represent the unique aspects of anxiety, another factor might represent the unique aspects of depression, and the third factor might represent the overlap between
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anxiety and depression. Such a hypothesis is consistent with other factor analytic studies in which anxiety and depression evidence unique and overlapping features (Ollendick et al., 1991; Williams et al., 1989), and with current theory in the adult literature. The Tripartite Model of Anxiety and Depression
A similar debate concerning the uniqueness of the anxiety and depression constructs in adults has led to the development of a tripartite model to explain the observed relationship between anxiety and depression. This model grew out of the identification of the construct of negative affectivity described by Watson and Tellegen (1985). On the basis of factor analyses with self-reports of mood data, Watson and Tellegen concluded that two factors, positive affect and negative affect, could best describe the basic structure of mood. More recently, Clark and Watson (1991) suggested a tripartite model to explain the similarities and differences between anxiety and depression. Simply put, the tripartite model suggests that anxiety and depression share a common component: high negative affectivity, and, more important, are differentiated by two distinct factors: positive affectivity and physiological arousal. High physiological arousal is specific to anxiety and low positive affectivity is specific to depression. The only direct test of the tripartite model in children and adolescents to date has supported the applicability of the model to youth (Joiner, Catanzaro, & Laurent, 1996). Additionally, testing the relevance of a tripartite model for cognitive symptomatology, Jolly and Dykman (1994) administered the Cognition Checklist (CCL; Beck, Brown, Steer, Eidelson, & Riskind, 1987) and self-reports of anxiety and depression to 162 children and adolescents between the age of 12 and 19 years, hospitalized for a variety of conditions including depression (47%), anxiety (2%), and conduct disorder (17%), among others. The CCL includes a depression and anxiety scale. Items from the CCL were subjected to an exploratory factor analysis in which three factors were extracted (this decision was made a priori in order to test the tripartite structure). Consistent with the tripartite model, one general factor included items from both anxiety and depression scales and accounted for 68.8% of the variance, a second factor consisted of only anxiety items and accounted for 11.4% of the variance, and the third factor consisted of only depression items and accounted for 5.7% of
the variance. Moreover, performing two separate multiple regressions, entering the factors simultaneously to predict self-reported anxiety and depression, the general factor and the specific anxiety factor, but not the specific depression factor, were significant predictors of the anxiety, whereas the general factor and the specific depression factor, but not the specific anxiety factor, were significant predictors of depression. Summary and Conclusions
In general, the literature suggests the distinctiveness of the anxiety and depression constructs. However, the number of studies, the lack of replication in different samples and the methodology used do not yet suggest firm support for either a unitary or binary construct model. In fact, mounting evidence points to the need for some compromise between these two models and, perhaps, a third model—the tripartite model. Despite the relative distinctiveness of the two constructs, there is also a great deal of overlap. Moreover, this overlap is evident even when repeated items used to assess anxiety and depression are eliminated. Despite the fact that confirmatory factor analytic techniques provide a means of testing the three competing models (i.e., the unitary model, the binary model, and the tripartite model), to date, few studies have employed these techniques. Further, evidence suggests that the relationship between anxiety and depression may be different for boys and girls (Williams et al., 1989) and across ages (Cole et al, 1997); however, few extant investigations consider these factors. ANXIETY AND DEPRESSION: COMMON RISKS?
A third possible explanation for the high rates of comorbidity between anxiety and depression in youth is that the disorders may share common risk/etiological factors. According to such a proposition, the fact that anxiety and depression share common risk factors, increases the probability that the disorders will co-occur. To demonstrate the plausibility of this third hypothesis to explain comorbidity between anxiety and depression, we must first examine the risk factors for anxiety that are risk factors for anxiety per se and not anxiety comorbid
132 Table III. Criteria for Accepting the Hypothesis that Comorbidity Between Anxiety and Depression in Youth is Due to the Overlap in Risk Factors 1. A set of risks common to anxiety and depression must be identified. These risks must be demonstrated to be risks and not simply correlates. The risk factors must be identified as being associated with anxiety and with depression not simply associated with anxiety because of its association with depression or the reverse. 2. The common risks should be found more often in those youth that evidence comorbid anxiety and depression than those youth that evidence pure anxiety or depression.
with depression (and the reverse) and demonstrate that some subset of these risk factors overlap with one another. Second it must be demonstrated that these risks are more common in groups of children that are comorbid with anxiety and depressive disorders than those who are purely anxious or depressed. A summary of these conditions can be found in Table III.
Risks for Anxiety and Depression Several areas of investigation, including temperamental factors, parent psychopathology, and cognitive errors/biases have been investigated as possible risk factors for development of anxiety and affective disorders. Although the literature is too vast to provide a comprehensive review, the following discussion highlights relevant findings.
Temperament Much research has been conducted to demonstrate the link between one temperamental factor, namely, behavioral inhibition to the unfamiliar, and the subsequent development of anxiety disorder. Behavioral inhibition has been described by Kagan and his colleagues (e.g., Biederman et al., 1990; Rosenbaum et al., 1988) as the tendency to be shy and cautious when exposed to unfamiliar or stressing stimuli and the inclination to withdraw from such stimuli upon their presentation. To varying degrees, several investigations have demonstrated that behavioral inhibition can be a precursor to anxiety. However, its specificity as a risk for anxiety is unclear.
Seligman and Ollendick For example, Rosenbaum et al. (1988) examined behavioral inhibition status in three groups at high risk for anxiety and/or depression: (a) children of parents with panic disorder with agoraphobia (PDAG), (b) children of parents with MDD, and (c) children of parents with PDAG and MDD. Additionally, a comparison group of children whose parents or siblings were being treated for other difficulties such as obesity (parents) or attention deficit disorder (siblings) was employed. Inasmuch as the children of parents with PDAG may be considered at high risk for development of anxiety disorder themselves, it was hypothesized that there would be a high rate of behavioral inhibition in these children. Most important for the discussion here is the comparison between the children of parents with PDAG and the children of control parents, which demonstrated a significantly higher rate of behavioral inhibition in the PDAG group. However, when rate of behavioral inhibition was investigated in the four groups, no differences were found among the offspring of PDAGonly group, the PDAG plus MDD group, and the MDD only group (although differences were in the hypothesized direction). Accordingly, the authors concluded that it is possible that behavioral inhibition may be a precursor to anxiety, depression, or comorbid anxiety and depression. A subsequent investigation more directly tested the link between the development of an anxiety disorder and behavioral inhibition (Biederman et al., 1990). Specifically, it was shown that normal children assessed at 21 months and classified as behaviorally inhibited showed higher rates of anxiety disorder (e.g., phobic disorder, SAD) between the ages of 7 and 8 years than those determined to be behaviorally uninhibited at 21 months. However, the only significant comparison was for phobic disorder, although there was a trend for behaviorally inhibited children to evidence a significantly higher rate of multiple anxiety disorders as well. No differences were found in the rate of MDD. However, a small sample was employed and only two children exhibited a depressive disorder, not unusual given the age of the children and the fact that depression often does not develop until adolescence (Zarate & Tbhen, 1996). It must also be remembered that the comparison group in this investigation was a group of uninhibited children, chosen to be at an extreme end of the inhibited/uninhibited continuum just as the behaviorally inhibited children were chosen for their extreme characteristics. Therefore, although these results can be interpreted as demonstrating a possible link between behavioral
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Anxiety and Depression inhibition and anxiety disorder, an equally plausible explanation could be that uninhibited children possess some protective factor. In the same investigation, when Biederman et al. (1990) compared inhibited children to simply not-inhibited children, they again found all rates of anxiety disorder were higher in the inhibited children but comparisons were not statistically significant (although, again, the sample for these comparisons and therefore power was relatively small). Another aspect of temperament, emotionalityactivity-sociability, was investigated by Rende (1993). Using a prospective design, he measured temperament at ages 1, 2, 3, and 4 years and behavioral/emotional problems at age 7 years and found that emotionality and sociability in infancy and early childhood were positively related to emotional problems (i.e., anxious and depressive symptomatology) in girls, but that emotionality alone was related to emotional problems in boys. Unfortunately, anxiety and depression were not measured separately; thus, no firm conclusions can be drawn about the specifics of the relationship of sociability and emotionality to anxiety, depression, or for that matter, anxiety and depression.
Parental Psychopathology Nonspecific links have been found between parental psychopathology and disorder in children. For example, S. M. Turner, Beidel, and Costello (1987) investigated psychopathology in children between the ages of 7 and 12 years of age of parents with an anxiety disorder (i.e., agoraphobia or obsessive-compulsive disorder), parents with dysthymic disorder, and parents without a disorder. Although they found children of anxiety-disordered parents were significantly more likely than children of non-disordered parents to manifest an anxiety disorder, rate of anxiety disorder was not significantly different in the children of anxious parents compared to children of dysthymic parents. Moreover, the disorders found in children of dysthymic parents were all anxiety disorders (SAD, OAD, and SP), demonstrating that both parental anxiety and parental depression (dysthymia) may be related to childhood anxiety. On the other hand, only one child (of an anxiety-disordered parent) met criteria for an affective disorder. However, again the sample was relatively small, and the oldest children in the sample were 12 years of age; therefore, children had not yet reached ages at which there is the greatest risk for affective disorders to be
present (Zarate & Tohen, 1996). Therefore, these data must be considered inconclusive in addressing the issue of the relationship of parental anxiety/depression to childhood depression. In a similar study, Weissman et al. (1984) found significantly higher rates of disorder in children of parents with MDD than in children of normal controls. Depression was the most prevalent (13.1%) diagnosis found in the children, but SAD (along with attention deficit disorder) was found to have the second highest prevalence rate, with 10.3% of the children of depressed parents evidencing SAD. Similarly, comparing children of normal controls with children of parents with recurrent depression, Orvaschel, Walsh-Allis, and Ye (1988) found a nonsignificant trend for the children of the depressed parents to have an anxiety disorder. Additionally, rate of anxiety disorder in second-degree relatives of the children of depressed parents was significantly higher than rate of anxiety disorder in second degree relatives of children of normal controls (Orvaschel, 1990). Last, as in Rosenbaum et al. (1988), Biederman, Rosenbaum, Bolduc, Faraone, and Hirshfeld (1991) compared risk of anxiety disorder in children of psychiatrically disordered parents (i.e., children of parents with PDAG only, children of parents with PDAG and MDD, children of parents with MDD only) with that of children with parents/siblings with other psychiatric disorders described earlier. They found children of the PDAG parents were at increased risk for anxiety disorder and at very high risk for MDD. However, contrary to findings from previous investigations, children of parents with MDD were not at increased risk for anxiety disorder, although they were at increased risk for an affective disorder. Not surprisingly then, children of parents with both PDAG and MDD were at increased risk for anxiety and affective disorders. Taken together, however, these studies suggest that both parental anxiety and parental depression are related to increased risk for both anxiety and depression in offspring.
Cognitive Biases Despite the prominent role of cognition as an etiological factor in psychopathology, few prospective studies, which are required in order to establish cognition as a risk/etiological factor, have been conducted. Furthermore, in a meta-analysis of attributional style and depression in children, Joiner and Wagner (1995) found little support from prospective
134 studies to suggest that cognitive variables actually predict future psychopathology. Accordingly, cognitions are best viewed as correlates of disorder not as risk/etiological factors (Gladstone & Kaslow, 1995). Even investigations that explore cognitive specificity as correlates of disorder find limited support. For example, Epkins (1996) examined the cognitive triad (i.e., negative view of self, world, and future) and cognitive errors/distortions in a group of socially anxious, dysphoric, socially anxious and dysphoric youth, and normal controls. Results indicated that all groups evidenced a more negative view of themselves, the world, and the future than normal controls. Further, examination of cognitive errors such as catastrophizing and selective abstraction revealed similar results. The content-specificity hypothesis (Beck, 1976; Beck, Rush, Shaw, & Emery, 1979) outlines clear similarities and differences for anxiety and depression. Although both anxious and depressed individuals should have disordered cognitions, according to this theory anxiety should be specifically related to cognitions centered around the theme of threat and depression should be specifically related to cognitions centered around the theme of loss. In a comprehensive investigation in children and adolescents, Ambrose and Rholes (1993) found these relationships to be more complicated than those suggested by the content-specificity hypothesis. Predicting depressive symptoms from anxiety cognitions, while partialing out the effects of depressive cognitions and anxiety symptoms, they found a significant curvilinear relationship between cognitions pertaining to threat and depression. More specifically, although it was true that at low levels of severity threat cognitions were not related to depression, as these cognitions increased in severity they became increasingly related to depressive symptomatology. Similarly, results revealed that cognitions pertaining to loss demonstrated a significant curvilinear relationship with anxiety. An inverted U shape best described the relationship between loss cognitions and anxiety, such that at low levels there was little relationship between loss and anxiety; however, this relationship increased as severity of loss cognitions increased, peaking at moderate levels and then decreasing again at the most severe levels. In sum, cognitive factors have not been well established as risk or etiological factors for anxiety or depression, despite theoretical assertions that they should be. Furthermore, even when viewing cognitions in terms of correlates rather than as risk factors,
Seligman and Ollendick there is not good evidence at this point to distinguish between distinct and overlapping features. That is, there are no cognitive variables that clearly emerge as related to anxiety only, depression only, and both anxiety and depression. Furthermore, similar cognitive styles have been found to be related to psychopathology in general (Joiner & Wagner, 1995).
Summary and Conclusions Although much interest and attention has been devoted to early identifiers of disorder and possible etiological factors, many of these investigations have found a lack of specificity in risk factors, such that risks can differentiate between children with and without psychopathology but are not specific to any one disorder (Anderson, Williams, McGee, & Silva, 1989). Additionally, many studies have chosen to investigate factors associated with risk for internalizing disorders more broadly (i.e., anxiety and depression), rather than anxiety or depression or they do not control for anxiety in those who are depressed or depression in those who are anxious. As such, it is difficult to determine which are the risk factors for anxiety versus depression. Thus, it is impossible at this point to identify a set of risk factors associated with anxiety only, depression only, and the set of risk factors that overlap. Although it is possible that all risk factors for anxiety and depression overlap, and thus contribute to comorbidity, this contention is difficult to defend since these same risk factors appear to be related to other types of psychopathology (Anderson et al., 1989). Accordingly, no clear conclusion can be drawn regarding comorbidity arising from common risks. Additionally, it may be the case that comorbidity between anxiety and depression occurs because of correlated rather than common risk factors, but again this is impossible to determine given the current state of knowledge. Moreover, several limitations of current research hinder our ability to proceed toward more definitive conclusions. For one, most studies have employed relatively small samples, particularly when investigating depression in childhood, resulting in inadequate statistical power. In addition, longitudinal investigations typically follow children only for a short period of time and assess youth in early to middle childhood or, at best, early adolescence. As a result, diagnoses of depression are often recorded when the children have not gone through the period of greatest risk for depression (i.e., adolescence).
Anxiety and Depression Therefore, the probability of false negatives is high, again decreasing the ability of these studies to identify risk factors specifically associated with development of depression. Additionally, studies of risk factors often do not account for comorbid conditions. Therefore, when a risk is associated with a certain disorder it may be that the association only exists because the disorder and the risk factor are both associated with a second disorder. In other words, one reason that the risk factors associated with anxiety and depression (and disorders in general) have been found to be the same is because the disorders are often comorbid and research typically does not control for this nor attempt to investigate risk in pure groups. Again, an adequate study of risk factors would need to employ very large samples in order to obtain adequate numbers of pure anxious and pure depressed and comorbid youth. Alternatively, comorbid conditions would need to be controlled for statistically. Last, much research on risk factors investigates relatively simple models in which a one-to-one correspondence is assumed. That is, these models implicitly assume that a risk factor such as parent psychopathology should lead directly to the development of one disorder, without sufficient regard to intervening variables. Current developmental theories suggest that this is improbable. Therefore, more complex, multivariate models of risk need to be developed and tested. Future research needs to focus on testing more complex models, in large samples of anxious only, depressed only, and comorbid anxious and depressed youth (or control for comorbidity statistically). Additionally, further investigations need to include older children and adolescents who have passed through (or are in) the period of greatest risk for depression.
DOES ANXIETY CAUSE DEPRESSION? Fourth, comorbidity may arise because one disorder causes or puts an individual at risk for the other. For such a hypothesis to be viable, it must be shown that anxiety precedes the development of depression and the outcomes of anxiety disorder can cause the development of depression or vice versa. For a summary of these criteria see Table IV Although an affective disorder may precede anxiety, in children and adolescents it is often found that anxiety precedes depression. Support for such a temporal relationship is found in both cross-sectional
135 Table W. Criteria for Accepting the Hypothesis that Anxiety Causes or Puts Youth at Risk for Depression 1. Anxiety disorders precede the development of the depression. 2. The outcomes of an anxiety disorder can cause/place one at risk for depression i.e., they match risk factors for depression). These outcomes must be demonstrated in samples that are not affected by depression in order to demonstrate the association with anxiety. The outcomes of anxiety must be demonstrated to be outcomes and not simply correlates. The risks for depression must be demonstrated to be risks and not simply correlates.
analyses and longitudinal findings. For example, Strauss, Last, et al. (1988) investigated the comorbidity of anxiety and depression in a sample of 106 anxiety-disordered children presenting for treatment at an outpatient clinic. The children evidenced a wide range of anxiety disorders including SAD, OAD, avoidant disorder, agoraphobia, panic disorder, SP, and obsessive-compulsive disorder. In all, 28% of the anxious children were found to be experiencing comorbid MOD. Comparing the anxious only and anxious and depressed groups on sociodemographic variables including sex, socioeconomic status (SES), age, and race, the only difference to emerge was that the youngsters evidencing both anxiety and depression were significantly older than their anxious only counterparts. Similarly, Strauss, Lease, Last, and Francis (1988) compared 23 children between 5 and 11 years of age to 32 adolescents between 12 and 19 years of age, all of whom were diagnosed with OAD. Results revealed that the older youth reported significantly more depressive symptomatology than younger children, even when the number of overanxious symptoms was controlled. Furthermore, similar to the Strauss, Last, et al. (1988) findings, adolescents were more likely to be experiencing comorbid MDD than children. Although differences were found for rates of comorbid depression in the two groups, the rate of comorbidity with other disorders was not different, with only three exceptions: comorbid simple phobias were more common in adolescents, SAD and attention deficit disorder were more common in children. Thus, the higher rate of depression in the adolescents is unlikely to be reflective of simply a greater level of psychopathology in general. Inasmuch as cross-sectional investigations can provide support for developmental phenomena, these data suggest that anxiety can lead to depression. However, more
136 definitive conclusions must be gleaned from longitudinal investigations. The recent increase in epidemiological investigations of childhood psychopathology, some of which have collected data for multiple waves, provides such evidence. For example, Feehan et al. (1993), examining adolescents from the Dunedin Multidisciplinary Health and Development Study, found that of the 15 adolescents diagnosed with multiple anxiety disorders at 15 years of age, around two thirds were found to have an affective disorder at age 18. For those with one anxiety disorder (OAD, SAD, or SP) at age 15, around one third had an affective disorder at age 18. Turning to a longitudinal study of clinic-referred children, Kovacs et al. (1989) found that 30 of 104 depressed children and adolescents between the ages of 8 and 13 years had comorbid MDD and anxiety. In about two thirds of these cases (n = 19), the anxiety disorder reportedly preceded the depression. Furthermore, the children with comorbid anxiety disorders were younger as compared to the depressed only children when they became depressed (mean age of onset for depression = 9.6 years), again suggesting that the presence of an anxiety disorder may lead to the development of an affective disorder. Thus, although several studies investigating the temporal relationship between anxiety and depression have been limited by their retrospective or crosssectional design, broad support exists for the assumption that anxiety precedes depression. However, the question remains as to how/why anxiety can lead to depression. One hypothesis suggests that the psychosocial sequelae of anxiety impact on the development of the child placing him/her at increased risk for depressive disorder. To demonstrate such a relationship it must be shown that the outcomes for anxiety disorder, not simply the outcomes for comorbid anxious and depressed youth, overlap with the risks for depression (see Table IV). One difficulty in establishing the effects of anxiety on the individual is that typically correlates of disorder are defined rather narrowly in terms of specific symptoms rather than more globally and with measures that may demonstrate significant impact on subsequent development. However, in an effort to establish the relevance of anxiety (and depression) as significant indicants of psychopathology, the associations between anxiety and social adjustment and anxiety and academic achievement have received increasing attention in recent years (Strauss, 1988).
Seligman and Ollendick Social and Academic Functioning in Anxious Children and Adolescents In general, findings suggest that anxious children are often socially neglected; that is, when their peers are asked to nominate children whom they like the least and like the most, anxious children do not receive nominations for either category. However, the results are not completely consistent (Strauss, 1988). Moreover, as will become apparent, findings are not readily interpretable for purposes of the present review. In a prospective study, Offord et al. (1992) found that youth with a diagnosis of an emotional disorder (i.e., features of DSM-III OAD, obsessivecompulsive disorder, and affective disorders) evidenced no more problems getting along with other children 4 years later than youth with no disorder at the initial assessment. Unfortunately, since this is one of the few prospective studies to examine this subject and, as such, one of the few studies that could shed light on the sequence of onset of disorder and social difficulties, Offord et al, assessed only for problems getting along with peers and not lack of interaction with peers or social neglect. Moreover, the youth who were examined evidenced features of both anxiety disorders and depression; however, it is unclear whether they would have met criteria for an anxiety and/or affective diagnosis. In a similar vein, Messer and Beidel (1994) found that anxiety-disordered children, who were either socially phobic or overanxious (with no concurrent diagnoses) did not perceive themselves to be less socially competent than normal controls. This is interesting given that about half of the anxiety-disordered group were diagnosed with SP and the anxious children did rate themselves as being less competent in other areas (e.g., physical competence). On the other hand, socially withdrawn children have been found to evidence higher levels of anxiety (Strauss, Forehand, Smith, & Frame, 1986). Using an observational method, Panella and Henggeler (1986) investigated the peer interactions of low-SES, inner-city, African American boys between the ages of 15 and 18 years. More specifically, they reported on the general domains of affect, amount of conflict, degree of dominance, and social competence and cooperation during a peer interaction task. Boys were placed in one of three groups: (a) conduct disordered, (b) anxious, or (c) well adjusted, based on information obtained from parents and teachers. Results revealed that anxious youth showed less positive affect when engaged in the social interaction task, were more apprehensive, and
Anxiety and Depression demonstrated less social competence. Although this investigation provides some evidence of social maladjustment in anxious youth, measurement of social adjustment and psychopathology was done at one point in time; as a result, there is no way to discern the sequence of events. In a similar investigation, examining the social behaviors of preschool children, Rubin and Clark (1983) found that children's frequency of unoccupied play and number of negative peer nominations was related to teachers' ratings of children's anxiety/fear. Also, in general, the children's level of anxiety/fear was correlated with solitary play. However, again it is impossible to determine if the social sequelae found were a result or cause of the anxiety experienced by the children because all measurements were obtained at one point in time. Similarly, Strauss, Frame, and Forehand (1987) investigated sociometric status and other peer perceptions of children rated as being either anxious/withdrawn or nonanxious/nonwithdrawn by their teachers. A total of 48 children participated, 24 in each group, with equal numbers of boys and girls included in the anxious and nonanxious group. In addition to matching on sex, groups were matched for grade and age. Results revealed anxious children were less popular than nonanxious children. Additionally, they were perceived by their peers to be shy and socially withdrawn (not surprising given that group status was partially determined by teachers' perceptions of withdrawn behavior) and less likable. However, again it is difficult to determine the direction of relationship between anxiety and social difficulties. Furthermore, the anxious children in this study reported high levels of depressive symptomatology; as a matter of fact, their mean score on a self-report of depression was within 1 standard deviation of the mean score for psychiatric samples with affective disorders. Thus, it is equally plausible that the social maladjustment observed was related to children's depression and not anxiety. In a more comprehensive investigation, Strauss, Lease, Kazdin, Dulcan, and Last (1989) investigated social competence in a group of 55 anxiety-disordered children between 5 and 17 years of age. The anxiety-disordered children were diagnosed with SAD (n = 12), OAD (n = 13), SAD and OAD (n = 17), simple phobia of school (n = 11), or other simple phobias (n = 2). They were compared to (a) a psychiatric control group: outpatients diagnosed with attention-deficit hyperactivity disorder, oppositional defiant disorder, conduct disorder, and/or adjustment
137 disorder, and (b) nonreferred children. Social competence was assessed using parent, teacher, and self reports. In general, self-ratings made by the anxious youth and the psychiatric controls were not different. However, anxious children rated themselves as lonelier and less socially competent than nonreferred children. Again, in most areas, parent reports for anxious children were no different than parent reports for psychiatric controls; however, parents of anxious children indicated they observed more withdrawn behaviors with their children than did parents of psychiatric controls or nonreferred children. Furthermore, parents of anxious children rated their children as having less appropriate social skills than parents of nonreferred children. Again for teacher reports, most comparisons between anxious children and psychiatric controls were not significant. In general, however, teachers rated anxious children as more shy, less socially skilled, and more socially isolated than non-referred children. Similarly, Strauss, Lahey, Frick, Frame, and Hynd (1988) assessed sociometric status of children between the ages of 6 and 13 years, with either OAD (n = 4), obsessive-compulsive disorder (n = 1), SAD (n = 3), or multiple anxiety disorders (n = 8). Again comparisons were made with a psychiatric control group (i.e., children with conduct disorder) and nonreferred controls. Children's classmates nominated the three children in their class they liked most, the three they liked least, and the three who fought the most. Anxious children received significantly fewer liked-most nominations in comparison with nonreferred children. Additionally, anxious children were more socially neglected than nonreferred control children, and they had less social impact. Although collectively these investigations provide some support for the contention that anxiety and social maladjustment are correlated, several methodological limitations preclude conclusions regarding more far-reaching implications. As evident in the foregoing discussion, with the exception of Offord et al. (1992), measurement of anxiety and social variables were taken at one point in time; thus, no conclusion can be made about the direction of the observed relationships. Obviously this is problematic when trying to draw conclusions regarding a developmental trajectory from anxiety and its outcomes to development of depression. Furthermore, the problem of comorbidity between anxiety and depression itself raises several questions about the proper interpretation of results of many extant investigations. For example of the
138 studies reviewed here, many either did not evaluate for depressive symptoms/diagnosis or did not report these results. Of those that did assess for depression, many found participating youth evidenced significant depressive symptomatology or an affective diagnosis. Strauss, Lahey, et al. (1988) conducted exploratory analyses (samples were small) comparing anxiousonly children and anxious and depressed children and found that anxious and depressed children received fewer liked-most nominations and were less popular than anxious-only children. This was true despite the fact that groups were equivalent in the severity of their anxious symptomatology. As a result, the authors suggested it may be depression associated with anxiety, and not the anxiety itself, that accounts for the significant relationships between anxiety and social outcomes. However, an alternative explanation may be that the anxious children who suffered from social neglect as a result of their anxiety went on to develop depression, whereas anxious children whose anxiety did not result in negative social consequences were less likely to develop a subsequent depression. However, the lack of available longitudinal data precludes us from choosing between such hypotheses. Indirect data, however, suggest that social functioning can impact later behavior and adjustment. For example, in the Waterloo Longitudinal Project, children were followed from age 5 into adolescence (Rubin, 1993). Results indicated that early social withdrawal was related to later internalizing symptomatology, including depression. Similarly, in the Social Competence Project, Ollendick and colleagues found that children rated by teachers as being socially withdrawn in fourth grade showed greater emotional difficulties in ninth grade than those youth who had been identified as well adjusted (Ollendick, Greene, Weist, & Oswald, 1990; Ollendick, Weist, Borden, & Greene, 1992). Similar to findings regarding social functioning, those concerning academic functioning are somewhat mixed, although most investigations conclude that anxiety does have a deleterious effect on academic performance. However, Gagnon, Craig, Tremblay, Zhou, and Vitaro (1995), for example, investigated the correlation between behavioral/emotional problems at age 6 years and academic performance at ages 10, 11, and 12 years and found no evidence of a relationship, although it should be noted that academic achievement was defined only in terms of appropriate grade placement.
Seligman and Ollendick On the other hand, Offord et al. (1992) found that emotional disorder diagnosed at ages 4 through 12 years was predictive of poor academic performance (as compared to children with no diagnosis at the initial assessment) measured 4 years later. However, emotional disorder was defined as features of DSM-III anxiety and affective disorders; therefore, it is difficult to determine whether these effects are associated with anxiety symptomatology per se. Moreover, academic performance prior to the onset of the disorder or even concurrent with the disorder (at the initial assessment period) was not controlled for in this analysis. Therefore, the direction of causation remains questionable. Similarly, in the Strauss et al. (1987) investigation described above, anxious children were rated by their teachers as having significantly poorer academic performance than nonanxious children. Again it must be noted that assessments were made at one point in time. Moreover, the fact that teachers rated both anxiety and academic performance and no objective indictor of academic achievement was obtained results in added difficulty in interpreting findings. In one of the most extensive investigations of this topic to date, lalongo, Edelsohn, WerthamerLarsson, Crockett, and Kellam (1994) assessed a total of 1,197 first-grade children enrolled in public schools in Baltimore, MD. Children's academic achievement (using a standardized group achievement test) and level of self-reported anxiety were assessed both in the Fall and Spring of first grade. Separate logistic regression analyses in which Fall anxiety scores were regressed onto Spring reading and mathematics achievement revealed that children whose anxiety scores were in the top quartile in the Fall of first grade were almost eight times more likely than the less anxious children to be in the lowest quartile for reaching achievement in the Spring and about 2!/2 times as likely to be in the lowest quartile for mathematics achievement in the Spring. Moreover, the regression analyses were conducted controlling for Fall level of reading/mathematics achievement and Spring level of anxiety; thus, providing relatively strong evidence that differences were the outcome of Fall anxiety. In addition, a recent meta-analysis supported the relationship between anxiety and poor academic performance (Seipp, 1991). Seipp reviewed a total of 156 studies conducted in several countries investigating the relationship between anxiety and academic achievement. She concluded that highly anxious children scored about one half a standard deviation below low
Anxiety and Depression anxious subjects on measures of academic achievement. Further, where possible, she investigated the relationship between the emotionality component of anxiety and the worry component of anxiety and found worry associated with anxiety may fully account for the relationship between anxiety and poor academic performance. Looking at sex and country as moderators, Seipp found an interaction between sex and country such that girls in the United States but not in other countries evidenced a stronger, more negative, relationship between anxiety and school performance. Therefore, in general, data suggest a link between anxiety and detriments in academic performance. However, the same methodological limitations discussed with regard to the literature linking anxiety and social functioning/outcomes apply here. Accordingly, so also do caveats regarding conclusions that can be drawn. Although, lalongo et al. (1994) made attempts in their analyses to investigate the direction of the relationship between academic performance and anxiety, and their results suggested that poor academic performance may be the result of anxiety, the remainder of the studies discussed can neither refute nor support such a conclusion. Furthermore, again it becomes unclear whether anxiety is related to academic performance or if they are connected because of a relationship with depression. Although children in the Offord et al. (1992) and Strauss et al. (1987) investigations reported depressive symptomatology, Gagnon et al. (1995) and lalongo et al. (1994) did not assess for depression in their participants. Likewise, although depression would have been an interesting and logical choice to investigate as a moderator in the relationship between anxiety and academic performance, Seipp (1991) neglected to consider depression in interpreting her meta-analytic findings.
Social and Academic Functioning in Depressed Children and Adolescents It has been hypothesized that, in addition to the risk factors discussed above, the inability or difficulty of an individual to emit behaviors that elicit positive reinforcement from the environment lead to depression (Lewinsohn, 1974). Specifically, Lewinsohn and his colleagues suggested that depressed children evidence social deficits and, as a result, do not receive positive social reinforcement. However, both boys and girls rate academic achievement as significantly more important to them than social performance
139 (Turner & Cole, 1994), suggesting that the feedback children and adolescents receive regarding their school performance may also be germane to the study of the development of depression. In fact, both academic and social impairment have been found to be associated with depression in youth. For example, Puig-Antich et al. (1985), studying children between the ages of 6 and 12 years, found those diagnosed with endogenous or nonendogenous depressions exhibited significantly greater levels of academic impairment than nondiagnosed children and psychiatric controls and significantly greater social impairment than nondiagnosed children. Additionally, depressed children have been found to be more socially withdrawn than psychiatric controls (Kashani, Vaidya, Soltys, Dandoy, & Reid, 1990). Using peer nomination procedures, Faust, Baum, and Forehand (1985) found children's selfreported depression to be negatively related to peer ratings of likability, children's perceptions of their positive nominations by peers (i.e., children's guesses as to the number of positive peer nominations they received), and children's perceptions of their likability ratings (i.e., children's guesses as to their peers' ratings of them). Moreover, they found self-reported depression to be positively correlated with negative nominations and children's perceptions of their negative nominations. A multiple regression analysis revealed children's estimates of their likability and negative nominations by peers to be the best predictors of depression. Unfortunately, no measure of social neglect was obtained. Similarly, examining social skill instead of social status, Vinnick and Erickson (1994) found parentand self-reported level of social skills to be negatively related to depression in third- and sixth-grade children. Furthermore, social skills appeared to interact with negative life events such that in the presence of high stress, social skill served as a protective factor, decreasing the likelihood of significant depressive symptomatology. In a somewhat more stringent test of the role of an academic stressor in the development of depression, Hilsman and Garber (1995) examined 203 fifth- and 236 sixth-grade children at three points in time. First, the children were assessed for depressive symptomatology 1 week prior to receiving their report cards. At this time, the children also indicated the lowest grade that would be acceptable to them for each subject. The children's depressive symptomatology was assessed again the day after and 5 days
140 after they received their report cards. Children's actual grades were recorded and academic stress scores were computed comparing children's reported acceptable grades with their actual grades such that academic stress was defined in terms of the degree of discrepancy between these two indices. Results indicated that at 1 day after receiving report cards, controlling for prior depressive symptomatology, academic stress was a significant predictor of self-reported depression. However, at 5 days after receiving the report cards, the academic stressor alone did not predict depressive symptoms. Rather the interaction of the academic stressor and children's academic cognitions (i.e., beliefs about their academic competence and ability to control academic outcomes) and the interaction of the academic stressor and attributional style (i.e., degree of internal, stable, and global attributions for negative events) did predict depression while controlling for previous depressive symptomatology. Similarly, poor competence in areas such as social and academic performance has been shown to predict the cognitive errors and attributional style associated with depression (Cole & Turner, 1993).
Summary and Conclusions Thus, although there appears to be some support for the fact that anxiety precedes depression, it is more difficult to determine whether consequences of anxiety can actually cause one to become depressed. Research is hampered by the lack of longitudinal investigations; thus, although it can be shown that social maladjustment and poor academic functioning are associated with anxiety and depression, the temporal sequence of events remains unclear. Additionally, the issue of comorbidity remains a problem in interpreting results. That is, when comorbidity is not controlled, either statistically or by using pure diagnostic groups, it is impossible to determine whether associations are due to the presence of an anxiety disorder, an affective disorder, or the combination of the two. Therefore, social maladjustment and poor academic functioning could be correlates/risks/outcomes of anxiety and/or depression! Accordingly, longitudinal investigations, controlling for comorbid conditions are needed to address these questions. Nevertheless, some intriguing conjecture can be offered at this point. For example, there appear to be differential social consequences for anxiety in boys and girls (Strauss, 1988). Similarly, there appear
Seligman and Ollendick to be different pathways from internalizing disorder for boys and girls such that boys are more likely to progress from an internalizing disorder to an externalizing disorder and girls are more likely to continue to experience internalizing problems (McGee, Feehan, Williams, & Anderson, 1992). However, the process by which these differential outcomes unfold has received little attention. Therefore, an interesting question for future research is to investigate these pathways more specifically and to determine if the different social sequelae for girls and boys contributes to the progression along different pathways. Additionally, it may be that the chronic sequelae of anxiety (if factors such as social maladjustment and poor academic performance prove to be outcomes of anxiety) can lead to both the diathesis and the stress proposed in many models of depression (Cole & Turner, 1993). For example, peer neglect could lead a child to develop negative views about him/herself, the world, and the future (i.e., the cognitive triad), in other words, a cognitive diathesis. In addition, continued incidents of peer rejection may provide salient stressors. Similarly, chronic academic failure could lead to cognitions regarding the uncontrollability of academic outcomes. Again, the continuing academic difficulties could also serve as stressors. Together these factors may precipitate the development of depression.
INTEGRATIVE SUMMARY AND CONCLUSIONS In sum, although tentative inferences may be drawn, it should be apparent that much remains to be done before these can be considered firm conclusions. First, examination of the definitions of anxiety and depression, both at the categorical and dimensional levels, suggests that symptom overlap alone cannot explain the comorbidity between anxiety and depression. It is likely, however, that symptom overlap plays a role, as can be seen by the extent of overlap in items on the GDI (Kovacs, 1985) and RCMAS (Reynolds & Richmond, 1978) and in the criteria for disorders such as GAD and MDD. Second, emerging evidence suggests anxiety and depression are not completely distinct constructs, nor are they two indicators of a unitary construct. Rather, anxiety and depression seem to share a common component (i.e., negative affectivity) and have distinguishing features (i.e., physiological arousal and low positive affectivity) as well (Clark & Watson, 1991). Thus, heavy reliance on the negative affectivity construct in the
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Anxiety and Depression definition of anxiety and depression may lead to the appearance of comorbidity. Third, little can be said about the possibility that common or related risk/etiological factors for anxiety and depression increase the probability of comorbidity. Currently, risks for psychopathology have been identified; however, risk factors specific to any disorder or class of disorders have yet to clearly emerge (Anderson et al., 1989). Last, correlates of anxiety and depression suggest the possibility that anxiety could lead to, or place one at risk for, a subsequent affective disorder. However, this is purely speculation since sufficient data to differentiate correlates from risks and outcomes are not yet available. Having drawn these tentative conclusions, several caveats must be issued. It appears the reasons for the comorbidity of anxiety and depression may not be fully explained by the characteristics of the disorders themselves. That is, conclusions drawn here may be further tempered by the fact that organismic or person variables also effect the relationship between anxiety and depression. For example, some data suggest that the distinctiveness of anxiety and depression is determined in part by the child's level of cognitive or emotional development (Cole et al, 1997). Therefore, although anxiety and depression may be best described by a tripartite model for older youth and adults, a unitary model may best describe the relationship between anxiety and depression for younger children. Further, the association between anxiety and depression may be complicated by characteristics such as sex/gender (Williams et al., 1989). Similarly, the psychosocial sequelae of anxiety may be different for boys and girls (Strauss et al., 1987); thus, suggesting the paths from anxiety to depression may also be different. Additionally, the four explanations for the comorbidity of anxiety and depression considered here and the literature used to evaluate them have, for the most part, been discussed in isolation from one another. However, it is probable that comorbidity arises because of a combination of these factors and, further, that they are not completely distinct or independent. For example, the lack of risk factors specific to anxiety and depression could suggest the possibility of a unitary model. However, the overlap in risk factors may also be affected by the overlap with which anxiety and depression have been defined. Alternatively, these risk factors may be risks for the development of negative affect rather than anxiety or depression per se. Similarly, the emergence of the construct of negative affectivity and the tripartite
model of anxiety and depression (Clark & Watson, 1991) must, to some extent, be affected by the overlap in the definition of the constructs. Therefore, while it can be seen that the current literature provides a base from which to begin drawing conclusions and asking questions, much remains to be done.
IMPLICATIONS AND FUTURE DIRECTIONS Assessment In part, the implications of this review for the assessment of anxiety and depression must depend on the purpose with which assessment is undertaken. For example, when the goal of assessment is to obtain a complete clinical picture, item overlap in assessment instruments probably does not detract from their utility. In fact, due to the relationship between anxiety and depression it makes sense to ask questions about depression when assessing for anxiety and to inquire about anxiety when assessing for depression. Similarly, items that tap negative affectivity rather than the specific features of anxiety and depression also provide useful information. Although it may not be their intention to do so, many current assessment instruments appear to assess for associated features (e.g., the RCMAS item "Other children are happier than I") and tap more heavily the negative affect construct than the constructs that distinguish between anxiety and depression. When the goal is to differentiate between anxiety and depression or to determine if a comorbid condition is present, current instruments may not be sufficient. One measure that may be taken is to eliminate item overlap in instruments; however, this must be done cautiously since some of these items may represent core features of either anxiety or depression. Alternatively, future assessment aimed at differentiating pure anxious, pure depressed, and comorbid conditions could begin to focus more on positive affectivity and physiological arousal in their definitions of depression and anxiety or to assess positive affectivity, negative affectivity, and physiological arousal separately. Likewise, limitations in assessment instruments suggest that anxiety and depression should be evaluated using multiple instruments and multiple informants. Moreover, since simply administering additional questionnaire instruments may lead to an increase in item overlap in the aggregated definitions of anxiety and depression, other avenues of assessment (e.g.,
Seligman and Ollendick
142 physiological assessment) need to be explored more fully and utilized more commonly in research and practice.
Treatment The findings discussed herein suggest two major implications for the treatment of anxiety and depres^ sion in youth. First, the relationship of negative affectivity to both anxiety and depression suggests that interventions aimed at negative affect may be successful in ameliorating aspects of the impairment associated with both disorders. Second, the possibility that the consequences of anxiety (e.g., social neglect) may lead to the development of a secondary depression, suggests that treatment should include a preventive component that incorporates interventions aimed at the sequelae of anxiety.
Research As can be discerned from the critique of the current literature, one basic advance needed in future research is simultaneous attention to a number of variables; thus, necessitating large samples. Additionally, a greater emphasis on longitudinal investigations is necessary in order to investigate the temporal sequence of the onset of disorders as well as the outcomes/risks for disorder. Moreover, the questions that have been raised by cross-sectional data indicating age differences (e.g., applicability of the tripartite model) could be investigated in terms of the developmental processes that may give rise to such findings. For example, cognitive and emotional development could be investigated as explanations for age-related findings. Assessment at the symptom level is needed to determine whether presence of symptoms that are common to anxiety and affective disorders is related to comorbidity. Furthermore, data on symptoms could be subjected to confirmatory factor analyses to test specific hypotheses regarding the underlying structure of anxiety and depression. Also, specific symptoms of anxiety and depression (e.g., worry) that relate to later outcomes (e.g., academic problems) could be explored in order to explain these pathways more fully. Additionally, more sophisticated models of risk, taking into account the process by which disorder develops should be examined. Such an investigation
would allow for prospective study of the link between social rejection/neglect and academic failure, cognitive style, and the development of depression which was speculated on previously. Similarly, rather than simply stating that parental psychopathology leads to psychopathology in offspring, intervening variables, such as the effects of parental psychopathology on parenting style, could be investigated and possibly linked to more specific outcomes. In conclusion, in the not so distant past internalizing disorders in youth received little attention (Ollendick & King, 1994). Recent years have seen great advances focused on the phenomenology of anxiety and depression in youth and their relationship with one another. The focus for the next generation of research needs to move beyond describing this relationship and toward explaining it. Much remains to be accomplished.
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