Abstract
Depression is one of the most prevalent mental disorders. Accordingly, treatment research has flourished; however, prevention efforts have lagged behind. The extant literature is reviewed on the relationship between anxiety and depression and the potential for childhood anxiety interventions to reduce the risks of secondary depression. Additionally, methodological issues and recommendations in the design of depression prevention programs are presented. Research appears to support the view that anxiety plays a role in the development of depression; yet, the nature of that role remains unclear.
Introduction
Depression is one of the most prevalent mental disorders and carries the fourth greatest burden of disease. Depressive disorders typically have their onset in adolescence with prevalence rates climbing through late adolescence. Recent research appears to suggest that these numbers may be rising among children and adolescents as well as adults. Fortunately, treatment research has flourished, and numerous treatments for depression have shown real promise in helping those with clinical levels of disorder. In addition to the success of antidepressant medications, the following nonpharmacologic treatments for depressive disorders have been deemed “well-established”: behavior therapy, cognitive therapy, and interpersonal therapy. Numerous others have been identified as “probably efficacious” (e.g., brief dynamic therapy, reminiscence therapy for geriatric patients, self-control therapy).
In recent years, attention has shifted from research on the treatment of mental disorders to research on prevention. Recent recommendations, reports, and priorities of federal agencies serve as evidence of this shift. Additionally, numerous researchers have suggested the need for early identification and prevention programs for mental health disorders, particularly depression and anxiety. Numerous universal, selective, and indicated depression prevention programs have been conducted (e.g., Resourceful Adolescent Program, Problem Solving for Life, Coping with Stress Course, Penn Prevention Project). Many of these prevention programs have an emphasis on both cognitive–behavioral skills components (e.g., cognitive restructuring, problem-solving skills training, behavioral activation) and interpersonal risk and protective factors (e.g., development of support networks, interpersonal skills). To summarize the literature, depression-prevention programs, similar in terms of intervention targets (e.g., cognitive factors, social problem-solving skills) but varied in design and methodology (e.g., number of sessions, case identification), have had somewhat inconsistent findings. However, collectively the studies are suggestive of the effectiveness of depression prevention efforts. Interestingly, but perhaps not surprisingly, the foci of these prevention studies overlap considerably with the intervention targets found in anxiety-prevention programs.
The Relationship Between Anxiety and Depression
Anxiety and depressive disorders represent the two most frequently diagnosed categories of disorder, each with extremely high health and social costs. Anxiety disorders, however, are considered to be the most common of all mental disorders. Lifetime prevalence rates of anxiety disorders range from 15% to 25%, while lifetime prevalence rates of depression range from 10% to 18%.
While both anxiety and depression evidence high rates of comorbidity with numerous disorders, each is most highly comorbid with the other. Rates of comorbidity between anxiety and depressive disorders have been reported to exceed 50%. The high rates of comorbidity appear to be found consistently in adults as well as children and adolescents. Additionally, severity of symptomatology and impairment appear to be worsened in the presence of comorbidity.
The high rates of comorbidity result in questions regarding the nature of the relationship between anxiety and depressive disorders. Several theories have been proposed that may be grouped into two broad classes of explanations: methodologic and etiologic. Methodologic explanations include selection and assessment biases. Selection biases may occur due to the fact that comorbid cases are more likely to be identified and treated. In addition, the highly correlated measurements of anxiety and depression, definitional overlap, and/or the high degree of symptom overlap (e.g., difficulty concentrating) may result in assessment biases leading to comorbidity.
More frequently, theorists cite several possible etiologic explanations. Anxiety disorders may represent causal risk factors for the development of depression. While some studies have been suggestive of a causal role, there is a need for additional research to assert this relationship with confidence. Others have suggested that anxiety and depression share similar biological, genetic, and/or psychological vulnerability factors and, thus, anxiety may be the prodromal phase for depressive disorder. Alternatively, anxiety and depression may be distinct disorders with distinct vulnerability and risk factors. A third perspective characterizes anxiety and depression as having both shared and unique components. Clark and Watson’s tripartite model, for example, holds that anxiety and depression share a nonspecific component of generalized distress as well as specific components of physiologic hyperarousal (anxiety) and low positive affect (depression). The model has been supported in adult as well as child and adolescent samples.
Anxiety as a Marker of Future Risk of Depression
The onset of anxiety disorders typically occurs during childhood or adolescence, whereas depressive disorders tend to have their onset in adolescence to early adulthood. An exception appears to be generalized anxiety disorder (GAD), which often has a later onset that is more typical of depressive rather than anxiety disorders.
Several cross-sectional studies have suggested that symptomatology of anxiety temporally precedes depressive disorders. This research supports the suggestion that anxiety serves as a risk factor for subsequent depressive disorders. However, cross-sectional studies often suffer methodological flaws including a reliance on retrospective reports of the onset of the disorder. Fortunately, several studies have employed longitudinal designs. In a study of 1037 participants from the Dunedin Multidisciplinary Health and Development Study, Caspi et al. found reticent, fearful children at age 3 to have increased risks of depression by age 21. Similarly, Pine et al. in a sample of 776 youths assessed at three time periods across 9 years, found fears at age 14 to be related to an increased risk for later depression. Woodward and Fergusson, in a 21-year longitudinal study of 964 youth, found the number of anxiety disorders in adolescence (ages 14 to 16) to be significantly related to the risk for major depression in early adulthood (ages 16 to 21). Using data derived from the same study, Goodwin et al. found anxious/withdrawn behavior at age 8 to be related to increased risk of major depression in adolescence and early adulthood, even after controlling for confounding social, childhood, and family factors. Similarly, Bittner et al., in a 4-year longitudinal community study of youth aged 14 to 24 at baseline (the Early Developmental Stages of Psychopathology [EDSP] study), found the presence of any anxiety disorder, especially GAD, to be associated with an increased risk for onset of major depressive disorder. This risk increased with baseline anxiety disorder comorbidity and severity and, importantly, remained significant after adjusting for nearly all disorders occurring before the onset of the anxiety disorder(s). The authors concluded that this latter finding suggests that anxiety disorders “make an independent contribution to the risk of onset of major depressive disorder among adolescents and adults.” Additional findings from the EDSP study revealed that less than 20% of cases diagnosed with an anxiety disorder in the cohort aged 14 to 16 years had ever experienced a depressive disorder. Within 2 years, this rate had doubled; within 5 years, the rate had jumped to over 50%. Given these findings, a logical next step is to determine whether reducing the incidence of primary anxiety disorders results in a reduction in the incidence of secondary depression.
Anxiety as a Target for Prevention of Depressive Disorders
The wealth of the data reviewed thus far has clearly established the high prevalence rates and significant social and personal costs of depression. Given the association and sequencing of anxiety and depression combined with the overlap in symptomatology, categories of risk factors, and treatment focus and technique, it appears that the prevention and/or treatment of anxiety disorders, especially childhood anxiety disorders, can serve as interventions for secondary depression. To support this argument, the research literature on the treatment of childhood anxiety, treatment of anxiety to prevent depression, and prevention of anxiety to prevent depression will be reviewed.
Treatment of Anxiety Reduces Anxiety
Cognitive–behavioral interventions have shown real promise in helping children with anxiety disorders. In fact, cognitive–behavioral treatments for anxiety disorders have been deemed “probably efficacious” as determined by proposed criteria. Notable is the overlap of treatment targets (e.g., cognitive restructuring, behavioral rehearsal, problem solving, social skills training) between depression-prevention programs and anxiety treatments.
Kendall conducted a randomized clinical trial including 47 anxiety-disordered children randomly assigned to either a cognitive–behavioral treatment or a wait-list control condition. Results indicated that 64% of treated children versus 5% of wait-listed children no longer had their primary anxiety disorder at post-treatment. Pre- to post-treatment effect sizes on child and parent reports of child anxiety and internalized distress were quite large (Cohen’s d 1.32 and 1.43, respectively). Follow-ups at 1 year, 3 years, and 7.4 years demonstrated maintenance of treatment gains.
Kendall et al. completed a second randomized clinical trial in which 94 anxiety-disordered children were randomly assigned to a cognitive–behavioral treatment or a waiting-list. Seventy-one percent of treated cases (vs 6% of wait-listed cases) no longer had their primary diagnoses at post-treatment. Again, pre- to post-treatment effect sizes were large (Cohen’s d 1.08 and 1.09 for child and parent reports of child anxiety and internalized distress, respectively). Maintenance of treatment gains was evident at the 1-year follow-up. Barrett et al., using a modification of Kendall’s Coping Cat program, added a family management component to the cognitive–behavioral treatment with good effects. Approximately 70% of treated children, versus 26% of wait-list children, did not meet criteria for an anxiety disorder at post-treatment. Pre- to post-treatment effect sizes were medium to large (Cohen’s d=0.74 and 1.12 for child and parent reports of child anxiety and internalized distress, respectively). One-year and 6-year follow-ups demonstrated maintenance of treatment effects. Several other researchers have documented the efficacy of cognitive–behavioral interventions for childhood anxiety.
Several researchers have adapted Kendall’s protocol for use in treating groups of anxiety-disordered children. Silverman et al. and Barrett compared a cognitive–behavioral treatment to a wait-list control. Results demonstrated that 64% and 65% of treated participants (vs 13% and 25% of wait-listed participants), respectively, no longer met criteria for their primary anxiety disorder. In the Silverman et al. study, pre- to post-treatment effect sizes were 0.65 and 1.42 for child and parent reports of children’s anxious distress, respectively. In Barrett’s study, pre- to post-treatment effect sizes were even larger (Cohen’s d averaged 1.95 across treatment groups for the child’s report of specific fears and 3.51 for the parents’ report of children’s internalized distress). In both studies, results were maintained at the 1-year follow-up. Flannery-Schroeder and Kendall compared individual and group formats to a wait-list control condition. Analyses revealed that 73% of individual and 50% of group (vs 8% of wait-list group) did not meet diagnostic criteria for their primary anxiety disorder at post-treatment. Pre- to post-treatment effect sizes were large (Cohen’s d averaged 1.26 and 1.34 for child and parent reports of child anxiety in the individual treatment, respectively; 0.73 and 1.23 for child and parent reports of child anxiety in the group treatment, respectively). Treatment gains were maintained at the 3-month follow-up. Similarly, Mendlowitz et al. found cognitive–behavioral group interventions to reduce symptoms of anxiety and depression in a sample of anxiety-disordered children.
Does Treating Anxiety Mitigate Depression?
Is it possible to reduce the risk for secondary depression via early treatment of anxiety disorders? Few studies have attempted to answer this question, and the existing studies on the topic have relied on retrospective reports (see Kendall et al. for an exception). Goodwin and Olfson, drawing on data from the National Comorbidity Study, evaluated respondents who “did” versus “did not” report receiving treatment for panic attacks in terms of their risk of developing major depression. Results suggested that 20% of those reporting treatment for panic versus 44.7% of those who reported no treatment developed subsequent major depression.
Kessler et al., also using data from the National Comorbidity Study, evaluated reports of temporally primary social phobia with respect to later diagnosis of depression. Active, ongoing social phobia was found to predict mood disorder occurrence while remitted social phobia had no effect in predicting first onset of mood disorder. Thus, the researchers concluded that early intervention in social phobia may lead to a reduction in subsequent depressive disorders, and this reduction may be as high as 10%.
Kendall et al. evaluated the long-term outcomes of children who received a cognitive–behavioral treatment for childhood anxiety disorders approximately 7 years earlier. While the study noted maintenance in anxiety at long-term follow-up, several anxiety disorder sequelae (e.g., depression, substance use) were also examined. Those participants who “did” versus “did not” receive an anxiety disorder diagnosis at post-treatment demonstrated less drug use and fewer negative consequences of drug use. The impact on depression was less clear. While there were no differences in diagnoses of depression between the two groups at the long-term follow-up, there was a trend toward reduction in depressive symptoms at the post-treatment assessment with a significant reduction at the 1-year follow-up and maintenance of these gains at the 7.4-year follow-up. Additionally, the current rates of depression at the 7.4-year follow-up—9.8% by parent report and 4.1% by adolescent report—approximate the rates found in the general population. The rates of a depressive diagnosis at any time since ending treatment were 32% by parent report and 23% by adolescent report. However, these findings are limited by the absence of a long-term control group. These studies, while not without limitations, are suggestive of the prophylactic effects of the treatment of anxiety on the risk of secondary depression.
Does Preventing Anxiety Prevent Depression?
Unfortunately, no published studies addressing this question appear to exist. However, research currently underway may provide some preliminary answers. A school-based indicated prevention study for children at risk for anxiety disorders (Promotion of Emotional and Behavioral Life Skills Project) being conducted by Flannery-Schroeder and colleagues, is a randomized controlled evaluation of the efficacy of group cognitive–behavioral intervention (GCBI) for children deemed at risk for an anxiety disorder(s). Ninety-eight children/adolescents aged 8 to 13, identified as “at risk” by a screening procedure involving the use of the Multidimensional Anxiety Scale for Children, are randomly assigned to either a GCBI or a smoking-education control (SEC) group. The intervention study is a 7-week between-subjects comparison on GCBI and SEC with evaluation of outcomes at post-intervention and durability of intervention effects and the impact on sequelae of anxiety (e.g., depression) at a 6-month follow-up. It is hoped that the results of this research can inform the literature regarding the possibility of preventing depression via the prevention of anxiety.
Designing Depression-Prevention Programs: Methodologic Considerations
Despite progress in the evaluation of programs designed to prevent depression, there remain significant limits in both the number and nature of the extant studies. Relatively few programs have been deemed effective and even those suffer from some significant limitations. Numerous researchers have introduced methodological considerations and proposed recommendations to remedy some of the existing problems in the current body of research. Many of these issues and recommendations will be reviewed here.
Participant Eligibility and Recruitment Issues
Given the nature of prevention research in which participants necessarily comprise a nonclinical sample, the determination of eligibility for prevention programs, in contrast with treatment programs, poses unique difficulties. For example, in the case of indicated prevention, identification of individuals evidencing subsyndromal or prodromal symptoms may be especially problematic. Most, if not all, mental disorders are believed to exist on a continuum from normalcy to clinical disorder. The line between “normal” demonstrations of depressive symptoms, for example, and subsyndromal symptoms of depression is certainly a blurry one. Additionally, incentive to participate is likely lower in prevention versus treatment programs as participants represent a nonclinical population. Participants may be unconvinced of their “need” for preventive efforts, unaware of their “at-risk” status, or unconcerned with their nonclinical (i.e., subsyndromal) presentation of symptoms of disorder. Furthermore, the comprehensive assessments preferred in prevention programs (see below) may represent a substantial burden for prevention program participants. Finally, depending on the type of prevention program employed, large sample sizes may make time and attention devoted to each participant minimal at best. This is especially true of universal prevention efforts.
Developmental Variability
Judgments about the timing of prevention programs should consider developmental stages and progression of disorder(s). That is, one must consider at what point preventive efforts should intervene in an individual’s life. In the case of depression prevention, do we intervene at the time of subsyndromal symptoms of anxiety, clinical levels of anxiety, or later subsyndromal symptoms of depressive disorder? Given what we know about the temporal precedence of these disorders, the ages at which individuals can be targeted may range from early childhood through early adulthood. Kendall and Kessler recommend consideration of a child’s social, cognitive, emotional, and interpersonal development before decisions regarding the timing of interventions.
Measurement Issues
Prevention efforts are longitudinal in nature. As participants age across interventions and follow-up periods, the latter of which may be quite extensive, the developmental appropriateness of the assessment measures should parallel the developmental growth of participants. While some child measures do indeed have corresponding adolescent and adult versions, few were designed or assessed for their continuity across developmental periods. Similarly, the developmental appropriateness of assessment measures may change across time. For example, the assessment of separation anxiety in childhood becomes increasingly irrelevant in adolescence and early adulthood, while the assessment of alternative symptoms such as panic may become more important.
Choice of assessment measures warrants considerable thought in prevention programs. Greenberg et al. note the “narrowness” of assessments in the existing prevention literature. Many prevention researchers have recommended the use of adjunct assessments to evaluate not only the intended direct effects of the prevention program but the potential indirect effects as well (i.e., “spillover” effects). To omit such assessments might obscure the possible secondary prevention benefits of the initial intervention. Additionally, assessment protocols should employ assessments of risk and protective factors in an effort to fully elucidate the etiologic nature of disorders under study. Even if a prevention program fails to demonstrate efficacy, the study can provide rich data on etiologic factors when using such comprehensive assessments. Finally, Clark recommends the use of measures of general functioning and/or quality of life as well as measures of positive behaviors and/or emotional well-being in order to assess both the impact and health promotion aspects of the intervention.
However, it is important to note that the large sample sizes in universal prevention studies may preclude the use of certain types of assessments (e.g., structured diagnostic interviews, behavioral observations). The lack of structured diagnostic interviews may have a secondary result, that is, a focus on prevention at the level of symptoms rather than disorders. While some researchers have noted this as a limitation, others believe that the assessment of symptoms to be an important first step. Gillham et al. note that the assessment of symptoms may not only be more feasible than the assessment of disorders but also may be justified due to the substantial literature documenting the association of high levels of symptoms and various negative outcomes.
Long-Term Follow-up
There has been a resounding call for long-term follow-up assessments in prevention research. Long-term follow-up is considered essential for several reasons. Greenberg et al. noted that some efficacious prevention programs demonstrated delayed preventive effects (i.e., positive effects evident only a year or more post-intervention). An absence of long-term assessments would obfuscate these late preventive effects termed “sleeper effects.” Alternatively, their absence might obscure findings that preventive effects are not maintained beyond some specified duration resulting in a missed opportunity to gain important information regarding timing of booster sessions and other remedial efforts. This leads to the question of the ideal interval for follow-up assessments. Researchers generally recommend that follow-up assessments occur at intervals long enough so as to occur after the period of elevated risk for secondary disorder(s). Current research reports follow-ups typically extending 1 to 6 years, but 15 years may be more appropriate for a valid assessment of potential preventive effects. However, the use of long-term follow-up assessments is not without inherent difficulties. A significant limitation in long-term follow-ups is the lack of control condition(s) associated with these assessment periods. It may be neither clinically responsible nor ethical to deny participants active treatments for such long time periods. Some researchers have attempted to sidestep this problem through comparisons of those for whom the intervention was successful versus those for whom the intervention was not. Last, in efforts to permit the completion of longer-term follow-up and to reduce the likelihood of participant loss for reasons such as inability to locate, Compton et al. have suggested that researchers secure permission early in the intervention project to contact participants in the future. This process leaves open the window for extending the number, and therefore duration, of follow-up assessments in preventive interventions that may have had neither the capacity nor the original intent to conduct them initially.
Conclusion
Research appears to support the notion that anxiety plays a role in the development of depression; however, the nature of that role remains unclear. For example, research has failed to definitively conclude that anxiety plays a causal role in the development of depression. Furthermore, it may be unnecessary and even theoretically impossible to answer questions of causality. More important is the need to assess the effects of interventions for anxiety on subsequent depression.
Childhood anxiety is likely not the sole pathway to adolescent and/or adult depression; however, it may be a pathway that is alterable when interventions for childhood anxiety are provided. Given the overlapping risk factors, high rates of comorbidity between anxiety and depressive symptoms and disorders, solid evidence of the temporal precedence of anxiety disorders over depression, and common intervention targets, it appears that the successful prevention and/or treatment of childhood anxiety disorders could markedly reduce the prevalence of secondary depressive disorders. In fact, some researchers have estimated that one quarter to one half of adult cases of psychopathology might be prevented by effective treatment of disordered youth. However, to date, prevention studies are limited in number and rarely target specific vulnerability/risk factors. They often suffer from narrow assessment batteries that fail to assess the trajectory of nontargeted problems. Prevention studies have typically neglected evaluations of an individual’s general well-being, giving priority instead to the assessment of specific symptom relief.
The present paper is a call for future childhood anxiety intervention studies that investigate the secondary effects on depression and future well-being more generally. Research appears to suggest that this approach may be fruitful in the prevention of depressive disorders, yet this remains to be substantiated by methodologically rigorous intervention studies. The time is ripe for such a call as participants in recent childhood anxiety intervention programs will soon enter adolescence and early adulthood. Without quick movement on this front, the window of opportunity to assess these effects will close.