Vulnerability to depression among adolescents: Implications for cognitive-behavioral treatment

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Vulnerability to Depression Among Adolescents: Implications for Cognitive-Behavioral Treatment Mark A. Reinecke, Northwestern University A n n e Simons, University of Oregon A range offactors, including early experience, parent-child interaction patterns, biological factors, and life events, have been associated with the development of depression among adolescents. Relations between early experience, attachment insecurity, and later depression may be mediated by failures to develop adaptive social skills, the acquisition of maladaptive beliefs or schema, or neurochemical factors (such as alteved hypothalamic~pituitary-adrenal response to stress, and changes in serotonergic, noradrenergic, and dopaminergic systems). Prevention and treatment models that attend to the fuU range of developmental, cog~zitive, social, and biological factors assodated with risk for depression are needed. Such models must account for observed increases in rates of depression during adolescence, as well as for gender differences in rates of depression that become apparent at that time. The Treatment for Adolescents With Depression Study (TADS) treatment protocol attempts to systematically address cognitive, behavioral, and social factors associated with vulnerability for depression among youth. It is a developmentally sensitive, formulation-based treatment model.

AJOR DEPRESSIONis a complex condition that is influenced by a range of factors (Akiskal & McKlnney, 1973, 1975; Garber & Flynn, 2001; Hammen, 2001; Ingram, Miranda, & Segal, 1998). When considering depression from a developmental perspective, several facts are worth highlighting. Depression rates among children are low. Recent epidemiologic studies indicate that 1% to 3% of children will experience an episode of major depression before the age of 13 (Cohen et al., 1993; Costello et al., 1996; Fleming & Offord, 1990). These rates begin to rise during early adolescence, followed by a dramatic increase between 15 and 18 years of age. By 18 years of age approximately 20% of teens will have experienced an episode of major depression (Lewinsohn, Hops, Roberts, Seeley, & Andrews, 1993; Lewinsohn, Rohde, & Seeley, 1998). This acceleration of incidence is especially pronounced for gins, such that a 2:1 ratio (equivalent to 28% for girls and 14% for boys) is well established by age 18 and persists through adulthood (Angold & Costello, 1995; Hankin et al., 1998; Lewinsohn et al., 1993). Many individuals experience their first depressive episode as an adolescent. Unfortunately, this first episode often marks the beginning of a longitudinal course of depression characterized by recurrent, disabling illness that is associated with psychosocial impairment across a number of domains (Lewinsohn et al., 2003; Weissman et al., 1999). Emslie, Rush, Weinberg, and Guillon (1997) reported that over 60% of depressed children experience a recurrence of their depression within 2 years. These facts

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Cognitive and Behavioral Practice 12, i 6 6 - 1 7 6 , 2005

1077-7229/05/166-17651.00/0 Copyright © 2005 by Association for Advancement of Behavior Therapy. All rights of reproduction in any form reserved.

underscore the need to understand adolescent depression, to address the question of why mid to late adolescence constitutes such a critical time period for the emergence of depression, why some teens experience multiple episodes, and to use this knowledge to develop more effective prevention and treatment strategies. One approach to answering these questions is to begin by- asking who is at risk for developing depression. Indeed, a rather long list of potential markers of vulnerability have been identified. Findings suggest that offspring of depressed parents are more likely to develop a mood disorder (Downey & Coyne, 1990; Kaslow, Deering, & Racusin, 1994; Mitchell, McCauley, Burke, Calderon, & Schloredt, 1989), and that subsyndromal depressive symptoms (Lewinsohn, Rohde, Klein, & Seely, 1999) or the occurrence of an anxiety disorder also increase the risk for developing major depressive disorder (Emslie et al., 1997). Negative life events have been shown to increase the risk for depression (Goodyer, Herbert, Tamplin, & Altham, 2000), as does being female. Although these factors serve as predictors of risk for developing a depressive disorder, they do not explain how the marker increases those chances or why this takes place during adolescence. From a prevention and treatment perspective, it would be helpful to know not just that being female increases the likelihood of becoming depressed but what is it about being female that raises the risk (Hankin & Abramson, 2001). In other words, what are the mechanisms and processes by which being female, experiencing stressful life events, or having a depressed parent translates into risk for developing depression, and which of these processes can be taken as targets of prevention and intervention efforts? Attempts to identify the mechanisms by which risk factors influence emotional adjustment have looked to envi-

Vulnerability to Depression ronmental factors (such as distal and proximal life events), developmental variables (insecure attachment style), cognitive variables (including dysfunctional attitudes or schema, problem-solving deficits, rumination, perfectionism, cognitive distortions, negative attributional style), family and social factors (such as social withdrawal, impaired conflict resolution, impaired communication, family interaction), and biological variables (serotonergic dysregulation; HPA axis reactivity). Unfortunately, m u c h of this research has been cross-sectional in nature. This is problematic insofar as many of these factors can also be viewed as predictors, concomitants, and consequences of depression. Social withdrawal, for example, may lead to depression due to its effects on opportunities for social reinforcement. It would, from this perspective, be a predictor or risk factor. Social withdrawal also, however, can be viewed as a symptom or correlate of depression, as well as a consequence of depression in that dysphoric individuals may behave in ways that alienate others. Studies indicate that depressed individuals may generate stressfnl events, which in turn may exacerbate and maintain their depression (Rudolph & H a m m e n , 1999). The child may internalize negative feedback from others as negative serfperceptions, which increase the severity o f the depressed m o o d (Cole, 1991; Cole, Martin, & Powers, 1997). Finally, social deficits associated with depression may place individuals at risk for recurrence or relapse. As Joiner (2000) cogently argued, clinical depression may be associated with a self-propagatory process of transactionally related psychological and behavioral processes that p r o l o n g and exacerbate symptoms and that increase the likelihood of recurrence. These processes are both cognitive and interpersonal in nature. Although his model was developed as a means of understanding the recurrent nature o f depression a m o n g adults, we have no reason to believe that similar processes may not be at play during childhood and adolescence. To be sure, m u c h of this approach is speculative. Questions c o n c e r n i n g t e m p o r a l relationships between these variables a n d depression (which may simultaneously serve as markers of vulnerability, causes, concomitants, and consequences o f depression) can best be answered through prospective, longitudinal research with both clinical and at-risk (albeit nondepressed) youth. It is possible that many of the variables identified as risk or vulnerability factors for the development of depression also may serve as mechanisms or process variables. Put another way, predictors or moderators may also serve as mediators of an outcome. Given the multiple and complex relationships between variables in contemporary diathesis-stress models o f depression, it is essential that scholars clearly articulate how variables of interest are associated with each other and with outcome. The articulation of a comprehensive model of adolescent depression must look beyond lists o f variables corre-

lated with adolescent depression a n d a t t e n d to the full range of factors implicated in the etiology and maintenance of the disorder. Such a model would describe how these variables transactionally interact over the course of development (Gotlib & H a m m e n , 1992; Spence & Reinecke, 2003). Insofar as risk or vulnerability factors may also maintain the disorder and place the individual at risk for relapse, they may serve as useful targets for therapy. Development occurs in a context. It is important from a developmental psychopathology perspective to attend to the tasks of each stage of development and the challenges each stage brings. O u r models of psychopathology and psychotherapy must attend to the social contexts in which adolescents function and develop. A broad and integrative diathesis-stress perspective provides a potentially useful organizational scheme for reviewing the developmental psychopathology of depression in adolescence and for relating this information to the treatment approach used in TADS.

Developmental Challenges and Stresses of Adolescence Puberty It has b e e n p r o p o s e d that h o r m o n a l a n d physical changes accompanying puberty may be associated with an increased incidence of depression. Studies indicate that weak associations may exist between estrogen levels and negative affect a m o n g girls (Brooks-Gunn and Warren, 1989; Susman, 1997). Research also has focused on a neuropeptide, oxytocin, whose levels increase during puberty. Extending this work to humans, Cyranowski, Frank, Young, and Shear (2000) suggested that increased levels of oxytocin may contribute to increased desires for interpersonal connection a m o n g adolescent girls. This increased desire for affiliation may constitute a vulnerability factor in that it may sensitize them to the disruption of relationships and interpersonal conflict, events that have been shown to predate depression in teens (Monroe, Rohde, Seeley, & Lewinsohn, 1999). O t h e r research has p u r s u e d the idea that for girls, pubertal timing--specifically early puberty, r a t h e r than puberty itself--may increase the probability of depression. Although the mechanism by which this might operate is unclear, the possibility exists that puberty and the resulting changes in physical appearance may highlight and intensify gender role expectations and stereotypes. Further, early maturing girls may be the recipients of awkward family and social reactions to their newly adultlike bodies, unwanted sexual attention a n d / o r pressure to engage in behavior that fits their appearance but not their level of emotional development, experience, or coping abilities. Given cultural pressures for thinness, the loss o f the pencil-thin silhouette of girlhood may be associated

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Reinecke & Simons with body image problems, another factor that is known to be associated with the d e v e l o p m e n t o f depression (Allgood-Merten, Lewinsohn, & Hops, 1990; Stice, Hayward, Cameron, Killen, & Taylor, 2000). All teens experience puberty, yet not all b e c o m e clinically depressed. Recent evidence indicates that while pubertal status predicted depressive symptoms in Caucasian girls, this relationship may n o t hold for African-American or Hispanic girls (Hayward, Gotlib, Schraedley, & Litt, 1999). This observation suggests that one must look to the other factors operating in an adolescent's life to understand the effects of puberty. Hayward et al. (1999) suggest that Caucasian, as c o m p a r e d to Hispanic and AfricanAmerican, culture places a particularly negative m e a n i n g to weight-related changes of puberty, a possibility that deserves further investigation. These puberty-linked vulnerabilities (e.g., increased reactivity to relationship disruption, negative evaluation o f puberty-linked physical changes, lack of skills required to deal with unwanted sexual attention) are addressed within the TADS protocol using skills of affect regulation, cognitive restructuring, and assertiveness training. Changes in Family and Social Network Adolescence is a time of social change. One of the developmental challenges of this period centers on shifts in family and social networks, a transition that can be stressful for some teens. With the increasing importance o f peer relationships comes the n e e d to cope with negative events such as an inability to join desired peer groups or consequences of affiliating with a negative peer group. Conflicts can occur as adolescents and their parents negotiate increased responsibility, independence, and privileges. Rueter, Scaramella, and Wallace (1999) have suggested that conflicts with parents stemming from increased i n d e p e n d e n c e may be implicated in the development of depression a m o n g adolescents. Negotiating this transition involves distantiation from parents, which may create conflict and anxiety in both parents and adolescents. These issues are addressed in TADS within the attachment, communication, and social skills modules. Changes in Educational Environment Adolescence also ushers in changes in the academic environment. The transition from elementary to middle school brings with it increased demands for social competence, planning and organizational skills, and flexible problem-solving, as well as greater expectations for performance. Academic responsibilities increase, and the importance o f developing educational and vocational goals becomes increasingly salient. At the same time, there is some evidence that negative associations may exist between academic performance and m o o d (Cole et al., 1996; F o r e h a n d et al., 1988; Ialongo et al., 1996). Depressed

mood, with concomitant declines in attention and motivation, may be associated with compromised academic achievement. The presence of a learning disability, or the lack of a g o o d fit between the needs and strengths of a child and the school setting, may contribute to feelings of dysphoria and reduced efficacy. Other Stresses and Negative Life Events Although adolescence is accompanied by a unique array of stressors, this does not mean that nondevelopmental events cease. Experiences such as parental divorce, death, loss, abuse, and unresponsive or neglectful parenting can occur and may play a role in precipitating the onset of depressive episodes (Compas, Grant, & Ey, 1994). Recent research by Cyranowski et al. (2000) revealed that over 70% of depressed females reported they had experienced one or more severe negative life events prior to the onset of their depressive episode. Interestingly, the corresponding n u m b e r for males was only 14%. Life events with interpersonal consequences have been f o u n d to be especially potent--approximately 95% of stressful events associated with the onset of a depressive episode were social in nature. Minor life events or "hassles" have also been associated with severity of depression a m o n g adolescents (Reinecke & DuBois, 2001). It is worth acknowledging that losses and stressful life events may not occur randomly across families. Divorce, for example, is associated with a range of stressors, including parental psychopathology, parental conflict, and marital violence. Moreover, the occurrence of a specific loss or traumatic event may foreshadow the occurrence of additional losses and stressors. A divorce or parental separation is frequently accompanied by a reduction in family income, a move to a new h o m e or school, and disruptions in relationships with peers and the extended family. It may not, as a consequence, be the occurrence of a specific loss or trauma that is associated with vulnerability for depression so m u c h as its association with an ongoing series of losses and stressors. Developing cognitive and behavioral skills for coping with major and m i n o r stressful life events are addressed in the problem-solving and social skills modules o f the TADS treatment protocol. Attachment and Depression Research with both h u m a n s and n o n - h u m a n primates indicates that the quality of early caregiver-child interactions can have important effects on later adjustment. Bowlby's ethological model of attachment provides a paradigrn for understanding these relationships. Vulnerability for depression, from this perspective, may be seen as stemming from early experiences in which the child's needs for security, nurturance, and comfort are not met. Bowlby (1969, 1973) proposes that consistency, nurturance,

Vulnerability to Depression protectiveness, and responsiveness in early interactions with caregivers contribute to the development o f working models of the self-in-relationship, and that these mental representations serve as a template for later relationships. Consistent with this model, evidence suggests that adverse early experiences can contribute to disturbances in early attachments that, in turn, may be associated with vulnerability for depression (Cummings & Cicchetti, 1990; Joiner & Coyne, 1999). Insecure attachment a m o n g children may be associated with negative self-concept, sensitivity to loss, and an increased risk of depression (Armsden et al., 1990; Batgos & Leadbetter, 1994; H a m m e n et al., 1995; Kenny, Moilanen, Lomax, & Brabeck, 1993; Koback, Sudler, & Gamble, 1991). Why might this be? Relations between attachm e n t security and depression appear to be mediated by the development of maladaptive beliefs or schema, at least a m o n g adults (Reinecke & Rogers, 2001; Roberts, Goflib, & Kassel, 1996; Whisman & McGarvey, 1995). The TADS p r o t o c o l attends to these findings by including an attachment-based treatment module that focused u p o n developing a reliable, supportive, responsive, and secure parent-child relationship. These interventions are based on two assumptions. First, we assume that the quality o f current parent-child interactions matter--the TADS treatment protocol attends to the proximal role of the family environment for adolescents' adjustment. Second, we assume that changes in attachment representations and associated beliefs may lead to clinical improvement (Sperling & Lyons, 1994). To be sure, one cannot presume that systematic relationships exist between attachment security during infancy and the quality of relationships during adolescence. Social adjustment during adolescence is multiply determined, and the stability and predictive value of measures o f early attachment security are, at best, modest. That said, indices of adult attachment style (which may usefully be viewed as measures of "attachm e n t cognitions") have been f o u n d to predict symptomatic response to interpersonal events ( H a m m e n et al., 1995). With this in mind, adolescents' beliefs and expectations regarding the reliability, supportiveness, and responsiveness of individuals who are important to them are seen as a useful focus for TADS treatment. The Effects o f Early Loss It has long been recognized that the occurrence o f traumatic losses and stressful events often precede the onset of depressive episodes. Relations between life events, chronic stressors, and mood, however, are complex (Mazure, 1998). The death or loss of a parent can be traumatic for a child, and can place them at risk for b e c o m i n g clinically depressed (Compas, Grant, & Ey, 1994). However, not all individuals who experience a loss or traumatic event develop the clinical syndrome of depression, and

not all adolescents who develop major depression report experiencing a precipitating negative life event. Attempts to understand individual differences in response to stressful life events suggest that (a) certain life experiences may have a more deleterious effect than others, (b) individuals differ with regard to vulnerability and the availability o f psychological and social resources t h a t may ameliorate or buffer against the effects of psychosocial stress, and (c) the context in which stressful events occur can influence their effect on adjustment (Dohrenwend & Dohrenwend, 1981; Hobfall &Vaux, 1993). The effects o f early parental loss appear to depend, for example, on whether this occurs due to separation, divorce, or death, and on how others in the child's life are affected by the loss. Outcomes may also be influenced by the age at which the loss occurs, concomitant environmental stressors, availability o f social supports, adaptive coping skills, and the effects o f the loss on the remaining caregiver. Brown (1988) proposed that there are two ways by which early parental loss may contribute to vulnerability for depression. The first involves the o n g o i n g occurrence of additional negative life events as a consequence of the early loss. It is the accumulation of stressful life experiences, then, that is believed to render an individual vulnerable for depression. The second path involves the establishment of enduring, maladaptive cognitive sets, impaired self-concept, and the failure to develop adaptive beliefs and coping skills. These maladaptive beliefs, attitudes, expectancies, and coping strategies, when activated by stressful life events, precipitate the onset of a depressive episode. The latter perspective, as such, forms the foundation for c o n t e m p o r a r y cognitive diathesis-stress models of vulnerability for depression. It is worth acknowledging that these approaches are not mutually exclusive. The possibility exists that cognitive and environmental factors make i n d e p e n d e n t and unique contributions to vulnerability for depression a m o n g youth (Reinecke & DuBois, 2001). As Gilmer and McKinney (2003) succinctly stated, these processes "may occur in parallel and cross-interact." Distinguishing the effects of distal vulnerability factors (such as early loss or maltreatment) from those o f proximal precipitants o f the depressive episode (including major and minor life events), Brown (1988) proposed that the specific nature o f the loss might n o t be as important as the experiences that precede and follow the loss. Early loss appears to act as a vulnerability factor for depression only in the presence o f other stressful events. Moreover, perceived control over stressful events can moderate their effects. Rutter (1971), in a discussion o f the effects of parent-child separations on later adaptation, distinguishes between "risk indicators" and "risk mechanisms." He proposes that the effects of early loss may be mediated by subsequent reductions in parental nurturance

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Reinecke & Simons and support, and on how this effects the child's developing views of themselves, their world, and their future. These, then, would be process variables and would serve as therapeutic foci in TADS CBT. In a provocative study, Harris, Brown, and Bifulco (1986) observed that poor parenting, even when not accompanied by the loss of a caregiver, was associated with an increased risk of later depression. In contrast, the early loss of a parent was found to be associated with increased risk for depression only when it was accompanied by impaired parenting. Taken together, these findings suggest that relations between early loss and depression may be due to ongoing effects of the loss on the child's social environment and developing belief system. In sum, stressful life events and parental loss are associated with risk for depression a m o n g youth. These effects appear to be influenced by the availability of social supports and perceptions of control. The accumulation of environmental stressors after an early loss may contribute to the development of increased feelings of hopelessness and decreased feelings of personal efficacy. Moreover, the lack of a supportive, nurturing relationship with a caregiver may lead to poor self-image. These self-referential processes may play a role both in the etiology of depression and serve as a mediator o f therapeutic change (DuBois, Lopez, & Parra, 2003). The TADS treatment protocols attended to these findings by including assessm e n t and treatment modules designed to enhance problem solving, improve social support, alleviate stress, and provide patients with perceptions of efficacy and control.

The Effects of Childhood Maltreatment Childhood maltreatment also is associated with an increased risk of m a n y forms o f psychopathology, including depression (Brown & Anderson, 1991; Kessler, Davis, & Kendlm, 1997; Paolucci, Genuis, & Violato, 2001). Although several forms o f maltreatment can be disting~aished--including physical, sexual, and emotional abuse, and neglect--they frequently co-occur. Moreover, as in the case of early parental loss, the effects of childhood maltreatment appear to be mediated by several factors. These include the severity, frequency and chronicity of the abuse, the specific nature of the mistreatment, the age of onset of the rnahreatment, the availability of social supports, and the availability of adaptive coping resources. A recent meta-analysis of 37 studies indicated that significant relationships exist between early sexual abuse and several forms of psychopathology, including depression (Paolucci et al., 2001). As the authors noted, however, there appears to be a "multifaceted model of transmission rather than a specific sexual abuse s y n d r o m e . . . " Although female victims of early sexual abuse are at an increased risk for later depression, victims of early sexual abuse also tend, as a group, to be more likely to have ex-

perienced other forms of parental violence and neglect. These other forms of abuse and neglect often predate the occurrence of the sexual abuse, suggesting that sexual abuse may tend to occur in a context of preexisting or ongoing parental neglect. Studies indicate that families of children who have b e e n abused manifest higher levels of conflict, marital problems, and parental psychopathology than do families of children who have not been abused. The possibility exists, as such, that it is not the acute episode of sexual abuse per se that is associated with vulnerability for later depression so m u c h as the o n g o i n g culture of neglect and impaired parenting in which the child is living. As with research on early loss and stressful life events, preliminary findings suggest that associations between abuse or maltreatment and m o o d may be mediated by the development of depressogenic beliefs. It appears, for example, that early emotional maltreatment might lead to the establishment of a negative attributional style, which in turn may be associated with vulnerability for depression (Gibb, Abramson, & Alloy, 2004; Gibb, Alloy, & Abramson, 2003). In conclusion, early abuse may be a risk indicator for later depression. Familial dysfunction may moderate this association. The effects of specific early adverse experiences and losses appear to be influenced by their impact on subsequent relationships and stressors and by" their effects on children's developing beliefs and competencies. A transactional system of risk factors may exist in which depression stems from the establishment o f a negative set of beliefs, attributions, and expectations that interferes with development and maintenance of supportive relationships. These, in turn, place an individual at risk for depression when a schema-congruent stressor occurs. The TADS treatment protocol attended to these findings by including assessment and treatment modules designed to improve parent-child communication, to reduce coercive parenting practices, and to actively involve the adolescent's parents in the treatment process.

Cognitive Vulnerability for Depression Contemporary cognitive diathesis-stress models propose that early adverse experiences h a m p e r the developm e n t of critical adaptive skills (including affect regulation and social skills), and contribute to the establishment of maladaptive beliefs and information processing styles (Garber & Flynn, 2001; Gotlib & H a m m e n , 1992; Spence & Reinecke, 2003). Depressed children and adolescents, like depressed adults, manifest negative views of themselves, their worlds, and their future. Moreover, they tend to demonstrate a maladaptive or negative attributional style, i m p a i r e d problem-solving, decreased problem-solving motivation, self-focused attention, a tendency to ruminate, perfec-

Vulnerability to Depression tionism, sociotropy or interpersonal dependency, and dysfunctional attitudes or schema (Gladstone & Kaslow, 1995; Gladstone, Kaslow, Seeley, & Lewinsohn, 1997; Hammen, 2001; Nolen-Hoeksema & Girgus, 1995; Reinecke, 2002). Studies suggest that measures of dysfunctional atfitndes may predict future depressive symptoms (Lewinsohn et al., 1994; Rudolph, Kuflakowsky, & Conley, 2001), and that measures of cognition and mood may be transactionally related. Feelings of dysphoria during childhood and early adolescence have, for example, been found to predict the development of negative beliefs about the self and the world, as well as declines in estimates of personal competence (Cole et al., 1999; Pomerantz & Rudolph, 2003). These negative beliefs and attitudes place the child at risk for further depression. Cognitive and perceptual appraisal processes, as such, appear not to be simple concomitants of depressed mood. Rather, they may mediate relations between stressful life events and feelings of depression (Kuiper, Olinger, & Lyons, 1986) and may be reciprocally related to mood. These findings are consistent with the observation that cognitive and perceptual biases, rather than "objective" measures of the severity of stressful life events, predict severity of depression among adolescents (Deal &Williams, 1988) and that the occurrence of early maltreatment, in conjunction with low self-concept and external locus-of-control, predicts severity of depression mnong adolescent females (Moran & Eckenrode, 1992). Specific TADS treatment modules focused upon identifying and alleviating cognitive and perceptual distortions, improving rational problem-solving skills and problem-solving motivation, and identifying and changing maladaptive beliefs. Affect regulation is dependent upon the acquisition and effective use of specific cognitive and behavioral skills or competencies, and has been characterized as a central developmental task of childhood (Bradley, 2000; Cicchetti & Toth, 1995). The development of affectregulation capacities, like other skills, occurs through supportive guidance and mentoring by parents and other adults. The development of these skills may be compromised in children who have been abused or neglected (Thompson, 1994), or who have been raised by parents who manifest psychiatric disorders, such as depression (Bradley, 2000; Cummings & Davies, 1994; H a m m e n , 1992b; H a m m e n , Burge, & Stansbury, 1990). Depressed youth demonstrate difficulties m a n a g i n g their emotions in distressing situations, showing decreased assertiveness and increased behavioral avoidance in comparison with controls (Koback & Ferenz-Gillies, 1995; Zahn-Waxlei, Klimes-Dougan, & Slattery, 2000). The TADS treatment protocol addresses this literature by including a treatment module focused upon developing affect-regulation skills.

Neurochemical Functioning Research indicates that the occurrence of stressful life events during critical periods of development can affect n e u r o c h e m i c a l functioning and can influence later m o o d and adaptation (Bremner & Vermetten, 2001; Graham et al., 1999; Helm & Nemeroff, 2001). Early adverse experiences have been associated with changes in catacholaminergic (DeBellis, Lefter, Trickett, & Putnam, 1994) and serotonergic (Kaufman et al., 1998) activity among youth. Early adverse experiences have been associated, as well, with changes in Hypothalamic-Pitnitary-Adrenal (HPA) Axis functioning. Elevated cortisol/DHEA ratios appear, for example, to be associated with increased severity of depression among adolescents (Goodyer, Herbert, Tamplin, & Altham, 2000), and cortisol hypersecretion may be associated with depression among prepubertal youth (Weller & Weller, 1988). Changes in HPA functioning in response to stress have been associated with early parental loss (Luecken, 1998; Weller, Weller, Fristad, & Bowes, 1990) and history of early abuse (Heim et al., 2000; Kaufman et al., 1997). Interestingly, observed relations between HPA reactivity and depression in the latter study were eliminated if the child was currently living in a stable home environment. Moreover, HPA axis activity may change over the course of the disorder (Puig-Antich et al., 1989). Although neurochemical activity appears to be associated with early loss, environmental stress, and mood, it may not be a stable predictor of risk. As Garber and Flynn (2001) recently remarked, "There currently is little evidence that HPA axis dysregulation is a stable vulnerability marker." These findings are important in at least three ways. First, they highlight the importance of viewing biological, social, cognitive, and environmental factors as part of an integrated adaptive system. Biological variables, from this perspective, do not play a "primary" role in the etiology and maintenance of depressive states. They are, at the same time, a cause, consequence, and concomitant of depressed mood, and exist in a transactional relationship with other vulnerability and risk factors. This perspective is consistent with recent work indicating that both stressful life events and the availability of social support moderate associations between serotonin transporter gene activity and depression (Caspi et al., 2003; Kaufman et al., 2004). In these studies possessing the short allele of the serotonin transporter gene (5-HTTLPR) was associated with the development of depression, but only when accompanied by a history of early maltreatment or stressful life events, or a lack of social support. These findings converge in suggesting that maltreated children and youth growing up in stressful environments are at an increased risk for depression, and that this association may be understood as reflecting a gene-environment interaction. Second, they suggest that we view psychosocial and phar-

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macological interventions as complementary. Psychosocial interventions, from this perspective, may exert effects on neurochemical functioning; and antidepressant medications may have effects on cognitive-perceptual processes. Finally, these findings direct our attention toward the central role of stress regulation in depression. The TADS protocol attended to this literature by including treatment modules that focused on relaxation training and on improving parent-child interactions at home.

Genetic Vulnerability for Depression Major depression appears, at least in part, to be a heritable condition (Beardslee, Versage, & Gladstone, 1998; Eaves et al., 1997; Harrington et al., 1993; Plomin et al., 1993; T h a p e r & McGuffin, 1994; Weissman et al., 1987). The effect sizes observed, however, are small, and (until recently) research in this area has not attended to geneenvironment interaction effects. As a n u m b e r of authors have noted, family studies tend to c o n f o u n d genetic contributions with the effects of a shared environment. Children raised in the same environment are often exposed to similar stressors, parenting, and social support. The specific "micro-environments" of children in the same family can differ, however, as can the ways in which these experiences are perceived or interpreted by each child. Genes do n o t function in isolation from the environment. Rather, environmental stressors activate gene expression at specific times (Bennett et al., 2002; Caspi et al., 2003). Gene expression and environment, as such, exist in a transactional relationship (Plomin, 1994; Plomin, DeFries, Craig, & McGuffin, 2003). Conclusion Although the TADS treatment protocol emphasizes the role of cognitive and social factors in the onset and maintenance of depression in y o u n g people, it is based u p o n a broader biopsychosocial model and looks for points of contact between the cognitive, social, and developmental psychopathology literatures. This kind of model provides a framework for understanding the developm e n t of depressogenic beliefs, attitudes, schema, and attributional styles, and the ways in which interpersonal and cognitive vulnerability factors interact with each other and with social-contextual variables and events to place individuals at risk for depression. Complex psychiatric disorders, such as major depression, appear to be multiply determined. A range o f factors appears to affect their onset a n d course, as well as response to treatment. Early experiences of loss or m a l t r e a t m e n t may interact with genetic vulnerabilities in placing individuals at risk for the development of depression. These effects appear to be mediated by subsequent stressors and social supports. Early life experiences, bio-

logical vulnerabilities, cognitive social environmental factors appear to transactionally influence one another in contributing to risk for depression a m o n g youth. The TADS CBT protocol is based, then, u p o n an integrative, multifactorial, developmentally based model of vulnerability for depression. From this perspective, earlyonset major depression is seen as a particularly pernicious condition. Depression during childhood and adolescence impairs the ability of the child to acquire important cognitive, emotional, and social competencies; it leads to the acquisition and consolidation of depressogenic beliefs, expectations and attributions; it damages current relationships and hampers the development of social supports; and it may lead to neurochemical changes and the activation of specific genes that contribute to depressed m o o d . Clinically, the m o d e l directs o u r attention to parent-child interactions, depressogenic schema and biased information processing, stressful life events, attachmentrelated beliefs, social skills, and affect-regulation capacities that may be implicated in the child's distress. This said, a n u m b e r of important questions remain unanswered. Do genetic, biological, or environmental factors play a more important role in the onset of the first depressive episode than in subsequent episodes? Do the effects of early life experience on risk for m o o d disorders differ a m o n g the affective disorders? That is, do risk factors for bipolar spectrum disorders differ from those for unipolar depression? Are there "sensitive" or "critical" periods during which stressful life events have an adverse effect on later affective development? How can we understand resiliency and the development of adaptive coping skills? How can we best understand the "microenvironments" that place individuals at risk for later depression? Do depressed youth (like depressed adults) behave in ways that have an ongoing effect on their relationships with o t h e r s - - d o they, in effect, create a "vulnerable environment" that increases the risk o f relapse? Do cognitive factors associated with vulnerability for depression tend to co-occur (a generalized maladaptive cognitive style), or do they make i n d e p e n d e n t contributions to vulnerability for depression? How malleable are maladaptive beliefs and attitudes associated with depression during childhood and adolescence? Depressed children and adolescents tend, like adults, to demonstrate depressogenic schema, cognitive distortions, a negativistic attributional style, and insecure attachment. How stable are these maladaptive beliefs and processing strategies over the course of development, and what factors account for their consistency over time? Answers to these questions will provide us with a foundation for understanding the ways in which cognitive, biological, social, and environmental factors interact in contfibuting to vulnerability for depression a m o n g youth and for developing even more effective treatment protocols.

Vulnerability to Depression The TADS CBT model has important practical implications. Research indicating that genetic and environmental factors may interact in placing youth at risk for depression, for example, directs our attention as clinicians toward (a) developing empirically supported interventions to improve parenting practices, and (b) actively working to improve social supports and social skills of atrisk youth. Along similar lines, research indicating that beliefs regarding the reliability, predictability, and supportiveness of others may be associated with risk for depression suggests that clinicians may wish to (a) carefully monitor teenagers' perceptions of the quality of the therapeutic relationship, (b) work to maintain a reliable and supportive therapeutic rapport, and (c) address negativistic thoughts that depressed teenagers may have regarding relationships with others. As noted, a n u m b e r of cognitive and interpersonal processes--including excessive reassurance seeking, conflict avoidance, and negative attention seeking--may be associated with relapse. Therapists will want to assess these behaviors and address them clinically. Assertiveness training, role playing of initiating social interactions, and negotiation skills can be helpful in this regard. In a similar manner, cognitive-behavioral interventions that serve to build an adolescent's self-concept may be useful in reducing the n e e d to seek reassurance from others. A n u m b e r of factors have been f o u n d to predict acute treatment response to CBT in the TADS project, including age, level of impairment at the outset of treatment, suicidality, duration of the depressive episode, level o f hopelessness, n u m b e r o f comorbid diagnoses, level o f anxiety, and the teenager's expectation that the treatment may be o f help to them. These findings are clinically useful insofar as they allow us to predict which adolescents will respond most favorably to CBT, at least in the short term. They also suggest ways in which clinicians might modify their therapeutic approach in order to facilitate rapid improvement. Attention might reasonably be directed during initial sessions toward alleviating feelings o f hopelessness a n d anxiety, reducing suicidal ideations, helping the patient to expect treatment success, and aggressively addressing c o m o r b i d behavioral and emotional problems. Research regarding predictors and moderators o f treatm e n t o u t c o m e in TADS suggest that some adolescents may be better able to benefit from TADS CBT than others. These findings challenge us to refine our treatm e n t protocols such that they are better able to meet the needs of adolescents who may not benefit from standard CBT. This would include adolescents who (a) are severely impaired by their depression, (b) have two or m o r e psychiatric diagnoses, (c) do not anticipate that treatment will be of value, (d) are acutely suicidal, (e) are from less affluent families, a n d / o r (f) are experiencing a more

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enduring (i.e., greater than 40 weeks duration) depressive episode. It is worth acknowledging that the TADS CBT protocol does not directly address a n u m b e r o f factors that may be associated with vulnerability for depression, including genetic and neurochemical contributions, early maltreatm e n t or sexual abuse, and academic difficulties. In practice, these concerns were m a n a g e d by allowing clinicians to refer patients for ancillary "non-TADS" services. There is an opportunity, then, to develop empirically supported treatments to address these needs such that the TADS CBT protocol will be m o r e effective as a m o n o t h e r a p y for a wider range of depressed youth. W h e n developing a treatment plan, clinicians typically focus u p o n identifying factors that may be maintaining their client's distress. As the astute reader will note, however, the TADS CBT protocol places an emphasis on understanding associations between factors associated with risk for onset o f the initial depressive episode. Many cognitive, social, and biological factors associated with onset and severity also have been f o u n d to be associated with clinical course, treatment response, and relapse potential (Goflib & H a m m e n , 1992). Lists of factors associated with each of these outcomes are, in fact, quite similar. With this in mind, research on vulnerability for depression may serve as a provisional guide for developing cognitive and behavioral treatment strategies. Contemporary theory, research, and clinical practice support the development of integrative, developmentally informed models of psychopathology and treatment. The TADS CBT protocol is based u p o n a model which recognizes that early-onset major depression is multiply determined, and that biological, environmental, social, and cognitive factors interact reciprocally over the course of development in contributing to risk. The model employed in TADS is conceptually sophisticated, and suggests a n u m b e r o f important directions for clinical and empirical exploration. Longitudinal studies are n e e d e d to explicate transactional relationships between factors within the model, as well as the ways in which factors associated with course, symptom severity, and risk for relapse can be addressed clinically.

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Received: March 8, 2004 Accepted: March 2, 2005 This article was accepted under the editorship of Anne Marie Mhano.