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Abstract

Objective: To review the characteristic clinical, illness course and risk factors to adolescent depression.

Method: A literature review is provided with interpretive comments.

Results: The clinical feature profile is likely to reflect the rarity of melancholic depression, while the non-melancholic ‘irritable hostile’ pattern appears distinctly increased. A ‘reactive depressive disorder’ is rare in those who get to psychiatric assessment, while comorbidity (e.g. anxiety and personality disorders, illicit drug use) is the rule. Aetiological determinants and the prognosis generally more relate to comorbid factors than to depression per se. Predisposing and precipitating psychological and social determinants are considered, while the efficacies of varying antidepressant strategies remain unclear apart from those withan ‘anxious’ or ‘irritable’ depression where selective serotonin re-uptake inhibitor medication has shown utility and where cognitive–behavioural therapy may be relevant.

Conclusions: For the majority who develop adolescent depression, its expression and outcome appear more a reflection of the propagating determinants, most commonly anxiety and personality style. The clinician should determine a treatment plan that not only addresses the depression but which identifies and addresses the contributing features.

Keywords

adolescent depression early-onset depression first-onset depression

A detailed review of childhood and adolescent depression [1] made two important statements about individuals born in the later part of the 20th century. First, that their chance of becoming depressed in adolescence has increased and, second, that first-onset depression is being manifested at a younger age than observed previously. Both may or may not be true, as destigmatization, increased training of practitioners, ‘depression awareness’ strategies and a range of sociocultural factors may have influenced reporting and preparedness to seek treatment, rather than there being a true increase in incidence and an age of onset advance. Any such trends apply more to mild-to-moderate depression, and seemingly not to the melancholic subtype [2], again arguing for sociocultural determinants of the reported changes. The growth in youth suicide has predictably alarmed the community and service authorities, further enhancing recognition of the need to address its determinants. In response, there has been considerable interest in developing programmes to prevent and address early-onset depression, with most focusing on prevention within high-risk groups (e.g. those with behaviourally inhibited temperaments; those exposed to sexual abuse, bullying and discordant families; those abusing drugs and alcohol). The literature base is expanding rapidly, providing an opportunity for preventative strategies to be developed and treatments to be implemented on a more rational basis, and encouraging the current overview.

In addressing the topic, the relevant review fields included depression in children and adolescents, as well as early-onset and first-onset depression. Rather than consider each as separate domains, we attempt to meld them and focus on depression in adolescence: although that focus requires some allowance in abstracting and interpreting the many studies reviewed. While early expressions of bipolar and unipolar melancholic depression are more common than generally recognized, both remain rare in adolescence, and will not be the subject of this review, despite the clear risk of adolescents developing bipolar disorder within 5 years of their first episode of major depression [3], [4].

Clinical features

The literature on clinical features is vast with a common preoccupation as to whether depression in adolescence and adulthood correspond. A recent Australian study [5] is informative in suggesting that features of adolescent depression do not differ distinctly from those of adult depression, apart from melancholic symptoms and psychomotor disturbance being rare: reflecting the rarity of melancholia in adolescents. The authors judged that loss of pleasure, anergia and fatigue, sleep disturbance, diminished concentration and suicidal ideation were of particular value in identifying ‘depression’ (as a disorder), while guilt, self-reproach, psychomotor change and appetite and weight change were useful markers of a more severe depression.

A noted feature of adolescent depression is irritability and anger [6–8]. This is of interest in light of the identification of a subgroup of ‘hostile and irritable’ depressed adults who experience anger attacks and have distinct psychological and neuroendocrine profiles [9], [10] and for which (see later) there is some suggestion of a different biological ‘type’. Such a pattern could merely reflect a common non-melancholic subgroup (i.e. ‘irritable hostile depression’) being overrepresented in adolescence, and either reflect the impact of immature psychosocial, cognitive and coping repertoires on clinical patterning or such a pattern being biologically destined to exceed threshold at an early age.

Natural course

Birmaher et al. [1] reported that epidemiological and clinical studies indicate that the onset of major depression (or its equivalent) is insidious for most, and acute for only a minority. Episodes tend to last 7–9 months on average, and while 90% remit within 1 to 2 years, the remainder experience distinctly longer episodes ordevelop ‘chronic’ depression. Thus, aggregated longitudinal studies indicate a 40% cumulative probability of recurrent depression by 2 years and 70% by 5 years. While rates of depression are similar for boys and girls during childhood, in adolescence, the proportion of depressed female adolescents increases to twice that of maleadolescents [11–13] and with determinants unclear. Postulates include an increased likelihood of anxiety disorders and ruminative response styles among girls, biological changes associated with puberty, sociocultural factors, and girls being more likely to experience stressful events asdepressogenic [14]. The difference has also been attributed to variations in the pathway to disorder status, with females being more prone to ‘act in’ (and so develop depression and anxiety) and males more likely to ‘act out’ (expressed behaviourally, and by use of drugs and alcohol). In regard to the last, clinical experience suggests that the literature may have failed to recognize recent ‘real world’ changes, with girls and young women increasingly engaging in so-called ‘externalising’ behaviours once viewed as the province of males (e.g. deliberate fast and excessive alcohol intake, one-night sexual stands, dangerous driving).

After recovering from depression, adolescents may continue to experience negative attributions, subclinical symptoms, impairment of interpersonal relationships and of global functioning [3], [15] associated with increased chances of smoking, early pregnancy [3], [16] and physical problems [3], [15], [16]. Those with lower socioeconomic backgrounds and educational levels [3] are vulnerable to recurrent episodes, as are those who develop their first episode at a young age [17]. However, while social difficulties in adulthood are generally more likely [16], if sustained recovery from depression occurs, adverse psychosocial deficits in adulthood are not necessarily increased [3]. It would be easy to conclude that such consequences are secondary to depression per se, but to the extent that anxiety and personality contribute to depression, such negative outcomes may more reflect the consequences and unfolding of those factors.

Dysthymia has been referred to as one of the ‘gateways’ to the development of recurrent mooddisorders [8], with early-onset dysthymia quantified as lasting for a mean length of 4 years, while distinctly increasing the likelihood of an episode of major depression within 2to 3 years of its onset. Adolescents with major depression superimposed on dysthymia (i.e. ‘double depression’) tend to have longer, severe and more recurrent depressive episodes, a higher rate of other disorders, a greater chance of suicide and more extensive social and functional impairment compared with those with either dysthymia or major depression alone [8], [18], [19].

Comorbidity

Identifying aetiological determinants is made more complicated by the rarity of depressed adolescents experiencing ‘pure’ depression [20–22]. The high rates of comorbid psychiatric disorders [3], [23], [24] lead to increased risks for recurrent and longer episodes of depression [3] as well as dictating a poorer treatment response [24–28] – but also obscure treatmentrecommendations [6].

Rates of comorbidity in association with depression have been estimated from 40 to 95% [6], with the most frequent being anxiety disorders [29–32] – including agoraphobia, social phobia, separation anxiety, overanxious disorder, enuresis, obsessive–compulsivedisorder – and dysthymic disorder [8]. The next most frequent disorders are ‘disruptive’ ones such as conduct or antisocial disorder and attention deficit hyperactivity disorder [33–36], personality disorders such as antisocial and borderline personality [37], [38] and substanceabuse [3] including nicotine dependence [39], [40]. Smoking, however, is commonly viewed as part of a pattern of acting-out behaviour linked to the development of antisocial and other personality disorders [41].

While the first episode of major depression is more likely to occur after the onset of other psychiatricdisorders [6], it generally precedes substance abuse by several years, with continued use of alcohol and drugs maintaining or worsening depressive symptoms [24], [42]. Depressed adolescents may develop conduct disorders as they seek to cope with depression, and such disordered behaviour may persist after the depressive episoderemits [33]. Conversely, signs of personality disorder may remit when the depressive episode remits, arguing for making any diagnosis of personality disorder provisional in depressed adolescents [27], [43] and only after assessing non-depressive functioning.

Depressive patterns comorbid with disruptive disorders have been held [44–47] to be a relatively distinct aetiological group, characterized by fewer melancholic symptoms, having lower familial aggregation of mood disorders, and the adolescents reporting more family criticism: factors favouring a psychosocial aetiology. Interestingly, while such individuals are more likely to respond to a placebo (perhaps suggesting more transient disorders), they have worse outcomes, less in regard to depression (where they experience fewer recurrences) but in experiencing higher adult rates of criminality and death by suicide. Thus, the antecedents and consequences appear more likely to relate to the disruptive personality style rather than to depression per se.

Adolescents with anxiety disorders who develop major depression have more persistent depressive episodes [24] are more likely to engage in substance abuse [48], [49] have more psychosocial problems and are more likely to have suicidal ideation [50–53].

Domains of risk factors

Candidate domains include predisposing familial and psychosocial factors, pre-existing psychopathology or antecedent disorders, and precipitating stressful life events. In addition to being risk factors to onset of the first depressive episode, risk factors such as comorbid anxiety disorder, lack of support, parental psychopathology, family conflict, exposure to stressful life events and low socioeconomic status also predict poorer response to treatment, suggesting their maintenance role. Several are considered separately.

Familial and genetic risk factors

Twin and adoption study evidence suggest that genetic factors account for some 50% of the variance in the transmission of mood disorders, with an additional impact also coming from the childhood familyenvironment – and which can vary due to individual members being treated differently by parents. In family aggregation studies, ‘top-down’ designs have identified higher rates of psychiatric disorders among the children of parents with depression, increased further when both parents have had episodes of major depression [54]. As parental depression increases the chance of a range of psychiatric and medical disorders [55], its specificity to depression remains to be determined. ‘Bottom-up’ family studies have identified depression prevalence ratesof 20–46% in first-degree relatives of depressed children and adolescents [56], with the highest prevalence being observed in relatives of those with early onset (< 20 years) depression [57].

Depression in adolescence (and childhood) is more likely [58] if the parent themselves had experienced early onset of their first depressive episode or recurrent depression, or if both parents evidence distinct psychopathology (e.g. one parent depressed and the other an alcoholic). The risk to both anxiety and depression is higher when both a parent and a grandparent have experienced depression [59]. Children of parents with panic or agoraphobia have been identified as having higher rates of anxiety and depressive disorders [45]. Thus, parental anxiety and depression appear to increase the risk of both conditions in children.

Sibling aggregation studies examining for risk of depression among offspring of depressed and non-depressed parents have found higher concordance rates for anxiety (as well as anxiety comorbid with depression) among offspring of depressed parents, particularly for parents who themselves have comorbid anxiety and depression, while a parental history of anxiety increases the chance of adolescent depression [54], [60].

Psychosocial family factors

An adverse family environment has an impact on increasing the risk of depression, suicidal ideation and suicidal attempts in adolescents [61]. Depressed adolescents tend to perceive their families as being more conflictual, rejecting, non-supportive and abusive [1], [62], with those in families with greater conflict experiencing higher rates of recurrence of depression. Causal postulates risk misinterpretation. Clearly, family conflict may be created in an otherwise normally functioning family by depressed adolescent [63], while family conflict may also be the result of parents attempting to control a child's disruptive behaviour [44].

Key parental contributions include behaviours and attitudes that increase insecurity in the child (and thus increase the chance of anxiety disorders) and promote a low self-esteem in the child [64], with both leading to decreased resilience to psychosocial stressors. ‘Chaotic’ family environments [58], whether structural (such as the mother living with a partner other than the biological father), or functional (such as family conflict) have been suggested as non-specific stressors that trigger depression in susceptible children [63], [65], [66]. Modelling by parents may also result in children not learning how to regulate negative affects, and in learning to ‘give up’ in the face of difficulties [67].

The role of the mother is regarded as particularly influential in the child's earlier years [62], [68], [69], while fathers may have greater impact when the child reachesadolescence [24]. There may be sex of parent–sex of child interactions, with one study [70] identifying females as more sensitive to the impact of uncaring mothering and males more susceptible to lack of care from their fathers. Methodological issues may cloud interpretation, particularly when mothers are more likely to be studied and rated than fathers.

Other indicative family factors that may increase risk of adolescent depression include lack of perceived social support [71], parental divorce [72], larger familysize [62] and older siblings with drug or alcoholdependency [62], [73]. Those who have been sexually abused are at increased risk of depression (in adolescence and in adulthood), although it has been suggested that any association may as much emerge from general dysfunctional characteristics of the family as from abuse per se [74].

Social factors

Any true recent increase in adolescent depression in developed countries has occurred during a period of political stability, in communities by and large untouched by war, and with social welfare systems providing the means of ensuring the basic necessities of food, shelter and clothing. At such times, according to Durkheim [75] and subsequent theorists, the community is more likely to develop anomic pressures, with internal cohesion lessened, creating a more depressogenic environment. How this might dispose adolescents to depression remains speculative but a number of factors are commonly nominated. Most appear to reflect on ‘societal values’, with an underpinning ‘moral value’ argument usually close to the surface. Thus, it is held that societal values currently emphasize a ‘self-focus’ of rights and freedoms, ignoring or minimizing ‘other-directedness’ and obligations to society. Second, that emphasis on non-responsibility for individual behaviours contributes to the individual viewing himself or herself as either not at fault or a victim, as responsibility lies with others. Further, the promotion of instant gratification (whether effected by sex, drugs and mobile phones) results in adolescents failing to learn to deal with frustration or to ‘do without’ and thus having less self-reliance and resilience. In addition, the decreased importance of the family unit and an increase in structural family problems (e.g. single mothers, an increase in divorce) continue to be nominated as contributing variables. Such changes are also implicated in the increase in drug taking by adolescents, which itself may contribute directly and iteratively to adolescent depression.

Behavioural and emotional risk factors

An ‘internalising’ style, such as being behaviourally inhibited, shy, anxious, dependent or a ‘worrier’, often links with cognitive preoccupations centring on unpopularity, insecurity and having a low self-esteem, so increasing the risk of depression in children andadolescents [62], [76]. By contrast, an ‘externalizing’ style more tends to increase risk for drug abuse and conductdisorders [62]. However, some externalizing behaviours, such as aggression, have been reported as risk factors to both depression and drug abuse. A lack of emotional reliance has been identified as a personality characteristic of adolescents prone to depression [77], [78].

‘Negative’ cognitive style

The contribution of such a cognitive style to adolescent depression has been studied extensively [71], [79], [80]. Components include a low self-esteem [81], self-criticism, perceived lack of control over negative events, negative attributions [11], [82], [83], hopelessness and a pessimistic style. Any such ‘negative’ cognitive style may be part of the endowed temperament, the consequence of adverse family and developmental factors, the product of modeling significant others, and even of repeated subsyndromal depressive experiences [67]. It has been shown in longitudinal studies of non-referred children to predispose to prolonged dysphoric moods after exposure to stressors such as a poor report card at school or rejection by peers [67]. It can also act iteratively, in that after a depressive episode, those with lower self-esteem levels (described as a lingering ‘scar’) are more likely to experience recurrent episodes [1] due to a greater chance of investing experiences with negative attributions.

Stressful life events

There appear to be modest associations between stressors in the year prior to onset of the first depressive episode [84]. Reported salient stressful events include loss of relationships with friends or parents, educational and work stressors, divorce of parents, bereavement, suicide by someone close – all being of greater moment when associated with other risk factors such as a lack of support [50],[85–87].

The recent breakup of a romantic relationship has been identified as increasing the chance of an initial adolescent episode, but not influencing risk of recurrence [88]. Although unemployment is associated with adolescent depression, it appears not to be a major factor per se. Thus, longitudinal studies have revealed that unemployment may reflect predisposing adjustment problems existing prior to school-leaving age, with longer durations of unemployment being associated with family social disadvantage, family dysfunction and instability and psychiatric disorder [89], and with all having their own capacity as risk factors to depression. Such a model (viewing stressors as triggering but not all explanatory) is likely to have wide relevance and help explain the modest contribution of stressful life events in quantitative studies.

Individual vulnerability to stressful life events varies considerably [90]. While the level of vulnerability tends to be enduring, environmental stressors can produce transitory but nevertheless significant effects [91]. Both the sensitivity or resilience to adverse events and the likelihood of exposure to them are believed to be partly genetically mediated [92], [93]. Evidence supports a personality dimension of ‘neuroticism’ as particularly mediating or defining this vulnerability [94], [95], with higher neuroticism levels a strong predictor of depression, via exposure to salient life events or via subjective weighting of such stressors. Thus, adolescents experiencing adjustment disorder with depressed mood in response to a stressful event appear at increased risk for major depression [37], indicating that life event stressors are better viewed as triggers in those with personality-based disposing vulnerabilities.

An integrative study

Most studies considered until now have contrasted those with adolescent depression to non-depressed control subjects. It is equally important to compare those with early-onset and late-onset depression, although the results are in broad agreement with the material presented earlier. We have contrasted [96] those experiencing early-onset non-melancholic depression (i.e. priorto 25 years) with those experiencing a later first episode. Despite being distinctly younger, the early-onset subjects had been depressed for a longer lifetime period, had had more episodes and been off work for a longer period. They did not differ in terms of depression severity or in clinical features of depression, but did differ in being distinctly more likely to report irritability, frustration, crankiness and loss of temper, and this pattern remained overrepresented after controlling for age. They were more likely to report a family history of depression, anxiety and alcoholism, but only somewhat more likely to report early structural family problems (e.g. raised by a single parent, multiple parenting) and did not differ in measures of parenting assessing care, control and abuse. They had higher lifetime rates of dependence on a range of illicit drugs (and benzodiazepines) and alcohol. They were more likely to have shown behavioural inhibition and school phobia in childhood, distinctly more likely to have had a lifetime anxiety disorder and to be judged by the psychiatrist as having a personality disorder, with both volatile and anxious worrying personality styles overrepresented.

Methodological problems

Despite much research into child and adolescent disorders, there is low agreement between reports of adolescents and of corroborative witnesses (e.g. teachers and parents). Adolescents are often resistant to interview, and tend to be more subjectively biased in presenting information and less ‘psychologically minded’ than adults, making data interpretation more difficult in undertaking studies. Much of the published data is cross-sectional and based on correlational analyses, making it difficult to establish causal relationships. Most studies focus on relatively narrow issues, making integration problematic. Many identified risk variables may be consequences, rather than antecedents of depression. There is considerable difficulty in determining whether a risk factor has any specificity to depression, or to a small set of disorders or is essentially pathoplastic in increasing the risk for psychopathology in general. True genetic influences may be missed, minimized and misinterpreted, while they may (as for developmental factors) ‘unfold’ over time due to age-related biological and psychosocial events. While ‘biological’ depressive disorders (e.g. bipolar depression, melancholic depression) rarely emerge in adolescence, any assumption of homogeneity to ‘depression’ can also confound study interpretation.

What are the clinical implications?

Adolescent depression is almost invariably nonmelancholic, with a clinical pattern of irritability being common (and which appears to continue across subsequent episodes). Such a pattern has been found [9] to be overrepresented in those with high levels of anxiety and a comorbid cluster B personality style, although our studies [Parker G et al.: unpublished data] suggestthat ‘irritability’ per se is better viewed as externalized anxiety rather than viewed as indicative of a cluster B style. Further, ‘irritable depression’ is associated with a decreased prolactin response to thyrotropin releasing hormone stimulation [10] (indicative of greater serotonin dysregulation) and responsive to selective serotonin re-uptake inhibitor (SSRI) antidepressant drugs. The high likelihood of a family history of anxiety, the early expression of behavioural inhibition or shyness and the high likelihood of having a lifetime anxiety disorder, suggest that high trait anxiety, anxious worryingand ‘neuroticism’ are possibly the most likely predisposing risk factors to adolescent depression. Presumably, higher levels of anxiety dispose to a set of consequences in addition to depression, including reliance on anxiolytic medication and illicit drugs, to cigarettes and alcohol, as well as impact on personality development, so accounting for much of the comorbidity described in the literature. Thus, clinical assessment and treatment should focus on identification of anxiety disorders. This is not always easy in adolescents when the boundaries between an anxious worrying style and ‘generalized anxiety disorder’ and between avoidant characteristics and ‘social phobia’ are often unclear, while many adolescents with obsessive–compulsive disorder deny (for guilt or other reasons) its existence. If medication is justified, the SSRI antidepressants appear helpful to many adolescentswith ‘anxious depression’ and ‘irritable depression’.

Other temperament style contributions to early onset depression are less clear. Depression in those with a volatile cluster B personality style does appear overrepresented in clinical practice, but it is not clear whether such individuals present because of their depression or because of other consequences of their personality style. A percentage of individuals with a perfectionistic and obsessional personality style may present at a young age, but in comparison with the prevalence of this style in the general community, it is probably underrepresented in clinical groups. The utility of antidepressant medication in these latter groups remains quite unclear.

The utility of non-pharmacological interventions (such as cognitive–behavioural therapy) may then be of distinct relevance to addressing some of the predisposing factors (such as behavioural inhibition) rather than being directed at depression alone. In reviewing the current state of knowledge perhaps the highest priority for attention is to establish the comparative efficacy and utility of available pharmacological and non-pharmacological treatments, and of the multiple primary preventative strategies that have been proposed.

‘Reactive depression’ may be extremely common in adolescents, but is rare in those presenting for psychiatric attention. Its excellent immediate and longer-term prognoses can be interpreted as allowing a more important conclusion: that for most who develop adolescent depression, outcome is more influenced by propagating personality and social world factors. Thus, the task of the clinician should be to determine a formulation that proceeds beyond details of the depressive condition and which tries to identify those contributing vulnerability factors amenable to intervention. Such an approach may have great utility for preventing the onset of future episodes and the distinct and often gravid secondary consequences of adolescent depression.

Footnotes

Acknowledgements

We thank MDU consultants, Heather Brotchie and Kerrie Eyers for constructive comments on this manuscript. This study was funded by an NHMRC Program Grant (993208) and an Infrastructure Grant from the New South Wales Department of Health.

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Adolescent Depression: A Review

Abstract

Keywords

Clinical features

Natural course

Comorbidity

Domains of risk factors

Familial and genetic risk factors

Psychosocial family factors

Social factors

Behavioural and emotional risk factors

‘Negative’ cognitive style

Stressful life events

An integrative study

Methodological problems

What are the clinical implications?

Footnotes

Acknowledgements

References