Interventions for Adolescent Depression
Abstract and Keywords
Rates of depression increase during adolescence and may put youth at risk for suicidality, future episodes, and impaired functioning in multiple life domains. Increased vulnerability for depression during this stage may occur because it is when the cognitive capacity for personal reflection, abstract reasoning, and formal operational thought develop; depressive styles for attributing events may hence form, along with hopelessness about the future. However, other biological and social influences may also interact with the increased cognitive vulnerability. Latino ethnicity and female gender appear to exert particular influence. Treatment for adolescent depression includes medication (mainly Prozac and Zoloft), cognitive-behavioral therapy, interpersonal therapy, and family therapy. Medication and psychosocial treatment is also combined, particularly for treatment-resistant depression.
Keywords: adolescence/adolescent, teenage/teen, depression/major depressive disorder, persistent depressive disorder, risk factors, evidence-based treatment, cognitive-behavioral treatment, prevention
While depression in children is relatively rare (2.8% of elementary-age children, according to Costello, Erkanli, & Angold, 2006), in adolescence there is a sudden spike in the rate of depression to rise to lifetime and 12-month prevalence rates of 11% and 7.5%, respectively (Avenevoli, Swendsen, He, Burstein, & Menkangas, 2015). The depressive disorders that pertain to adolescents are catalogued and described in the Diagnostic and Statistical Manual of Mental Disorders (DSM), published by the American Psychiatric Association (APA, 2013). The DSM is the standard resource for clinical diagnosis in the United States. Major depressive disorder is represented by at least a two-week period during which a person experiences a depressed mood or loss of interest in nearly all life activities with five or more symptom categories being represented. Persistent depressive disorder represents a general personality style featuring ongoing symptoms that are similar to, but less intense than, those of major depression. Disruptive mood dysregulation disorder is a 12-month pattern of behavior that is experienced daily of temper outbursts and irritable and angry mood starting before the age of ten. Disruptive mood dysregulation disorder is a new diagnosis created in DSM 5 to take the place of bipolar disorder that was being overly used with youth. Very little writing and research has taken place on this diagnosis as of this point, and, since it is quite different from the other depressive disorders, the focus will remain on depression as exemplified by major depression and persistent depressive disorder.
Some of the differences in categorizing major depressive disorder for youth are named in the DSM. Irritable mood is a criterion for youths but not for adults. The weight loss criterion is not used with children, because children and adolescents are continuing to develop physically and are subject to weight fluctuations regardless of mental status. The DSM specifies, however, that youths can meet the appetite and weight disturbance criteria by not sustaining normal standards of growth and weight (American Psychiatric Association, 2013). As well as some of the special considerations noted in the DSM, a greater reliance on collateral reports from parents and teachers may be necessary (Waslick, Kandel, & Kakouros, 2002). A symptom may be counted as present if either the parent or the child reports its existence.
The theories that explain the onset of depression and the factors that influence its occurrence will be discussed from a biopsychosocial perspective.
Nantel-Vivier and Pihl (2008) explored neurobiological origins of depression, which are various in nature and include structural and functional brain anomalies, hormonal changes, and neurotransmitter systems, as well as the interaction between biological vulnerabilities and environmental stress. Major depression tends to run in families, which supports, at least in part, a process of genetic transmission. Genes can predispose individuals to major depressive disorder in various ways. They help control the metabolism of neurotransmitters, the numbers of particular types of neurons and their connections, the intracellular transmission of neuron signals, and the speed with which all of these activities take place in response to environmental stressors. The serotonin transporter gene is the most studied in major depressive disorder. A shorter variation of this gene is believed to slow down the synthesis of the serotonin transporter, which reduces the speed at which serotonin neurons can adapt to changes in environmental stimulation. Given that an acute stressor increases serotonin release, this variation may influence a person’s sensitivity to stress (aan het Rot, Mathew, & Charney, 2009). Dunn et al. (2011) looked at 16 studies, focusing on gene–environment interactions to the risk of child and adolescent depression, and found at least one significant gene–environment association in 80% of studies. Further, stressful life events may increase the reactivity of the hypothalamic-pituitary-adrenal axis and the release of cortisone, which, over time, may lead to structural changes in the brain (aan het Rot et al., 2009).
Based on a meta-analysis of five twin studies, the variance explaining the heritability for major depression is significant, in the range of 31% to 42% (Sullivan, Neale, & Kendler, 2000). Interestingly, when Lau and Eley (2008) reviewed genetic studies involving youth and depression, they found that adoption studies have not replicated the family and twin studies. In sum, the biology of depression involves a complex and reciprocal process of the interrelated systems of the brain, about which much remains unknown. This explains why treatment with antidepressant medication, which targets only certain neurotransmitters, often does not lead to symptom improvement.
Germane to the discussion of biological risk factors, Cairns, Yap, Pilkington, and Jorm (2014) conducted a systematic review of longitudinal studies to identify risk and protective factors for adolescent depression that are modifiable. Risk factors associated with the biological level included substance use (alcohol, tobacco, cannabis, other illicit drugs, and polydrug use), dieting, and being overweight. Biological protective factors involved healthy diet and sleep (Cairns et al., 2014).
At the psychological level, theories have centered on cognitive factors; these include attributional theory, Beck’s cognitive theory of depression, and stress and coping theory (Abela & Hankin, 2009). Increased vulnerability for depression may occur in adolescence because it is a time of life when the capacity for personal reflection, abstract reasoning, and formal operational thought develops. At this stage, youth can first consider causality for the events in their lives, and they may develop a depressive attributional style (Abramson, Seligman, & Teasdale, 1978). This style attributes negative events to internal, stable, and global attributions (“I failed the test because I was stupid”), while positive outcomes are ascribed to external, transient, and specific reasons (“I passed the test because it was easy”). Adolescence is also a time in development when a future orientation develops; with this ability, the adolescent may experience hopelessness about the future (Abela, Brozina, & Haigh, 2002).
Another theory of depression involves Beck’s conceptualization of the role of thoughts in the development of depression and how cognitions affect feelings and behavior. Beck identified the “cognitive triad” of depression: thoughts about the self as worthless, the world as unfair, and the future as hopeless (Beck, Rush, Shaw, & Emery, 1979). Given these thought patterns, depression may arise and become entrenched. The theory of change is that people can become aware of this type of thinking and replace it with more realistic patterns. Treatment models arising out of cognitive theory are discussed later.
Compas, Jaser, and Benson (2009) integrated stress and coping theory along with the role of emotion regulation and identified both helpful and unhelpful coping mechanisms. For situations that are not in a person’s control, distraction and acceptance of a negative situation, maintaining an optimistic yet realistic outlook, and/or re-appraisal of the stressor can be beneficial. The strategies of rumination and searching for reasons behind negative emotions were identified as problematic (Compas et al., 2009). Rumination is defined as the tendency to focus on the symptoms of a poor mood, mulling over the reasons for its occurrence in incessantly, passive ways rather than in an active, problem-solving manner (Nolen-Hoeksema, 2002). To lend recent empirical credence to the role of negative coping, the systematic review of longitudinal studies of modifiable risk factors also identified negative coping as contributing to depression (Cairns et al., 2014).
Family factors include family functioning and the parent–child relationship, as well as maternal depression. In an excellent review of these factors, Rudolph (2009) discussed insecure attachment of the child and maternal depression setting the stage for poor interpersonal functioning and subsequent depression. Depression, in turn, leads to further interpersonal problems and risk for recurrence. A recent systematic review on family risk found that depression in youth was associated with conflict between parents, lack of parental warmth and aversiveness, overinvolvement, and both lack of ability to provide autonomy to children and lack of adequate monitoring (Yap, Pilkington, Ryan, & Jorm, 2014).
Abuse is discussed in this section as it usually occurs in the context of the family. A meta-analysis by Infurna et al. (2016) estimated the associations between depression and different types of childhood maltreatment, finding that psychological abuse and neglect were most strongly associated with the outcome of depression. Sexual abuse, although a significant risk, was less strongly related.
Depression in mothers is a particular risk factor for youth depression for many possible reasons. First, genetic factors may be involved (Goodman, 2007). Other biological factors may include the abnormal neuroendocrine functioning found in women who are depressed during pregnancy. As a result, the fetus may be exposed to increased cortisol levels and experience a reduced blood flow, leading to slower growth and less movement. Psychosocial explanations have also been posited (Goodman, 2007). Maternal needs for nurturing and care can interfere with a mother’s ability to meet children’s emotional and social needs. Mothers may be emotionally unavailable and feel a sense of helplessness in the midst of parenting challenges. Parents may model depressive affect, thinking patterns, and behaviors for their children and then reinforce their children’s depressive behaviors. Depressed parents also tend to see their children’s behavior in a negative light, using low rates of reward and high rates of punishment or responding indiscriminately to the child’s behavior.
While rates vary by study (Merikangas, Nakamura, & Kessler, 2009), a replicated finding is that Latino ethnicity is associated with a greater risk of depression compared to other U.S. ethnic groups (Allen & Astuto, 2009). Similarly, in the Twenge and Nolan-Hoesksema (2002) meta-analysis of studies of teens taking the Children’s Depression Inventory, Latino youth had elevated scores compared to either white or African American samples. Further, according to the Centers for Disease Control and Prevention (2011), rates of suicide attempts among adolescent Latinas are significantly higher than their Caucasian and African American counterparts.
Hypotheses suggested for these higher rates include the stress of acculturation; language barriers; being raised by parents who are immigrants who may suffer from poverty, unemployment, and depression themselves; and cultural factors, such as fatalism and an external locus of control (Allen & Astuto, 2009). In a study of risk and protective factors for Latino adolescent depression, males who were more oriented toward mainstream culture were possibly more vulnerable to the effects of discrimination (Umana-Taylor & Updegraff, 2007). Conversely, a high level of involvement in Latino culture may act in a protective way, since then discrimination may not affect their feelings of self-worth and depression. Acculturation was also highlighted in another study (Cespedes & Huey, 2008). Specifically, a discrepancy between gender role expectations among Latino teenagers and their parents was associated with depression, particularly among girls.
Another consistent finding is the greater risk for depression in females that emerges in adolescence (about age 13) and persists throughout the life span (Merikangas & Knight, 2009). Hilt and Nolen-Hoeksema (2009) reviewed the 2:1 differences in depression between females and males that start at about age 13. Not only did females experience a higher incidence of depression, but episodes were also more chronic (Essau, Lewinsohn, Seeley, & Sasagawa, 2010).
Various reasons, including the biological and the psychosocial, have been hypothesized for the gender gap in depression. Biological factors include reproductive hormonal development in girls—specifically estradiol, the primary female sex hormone, which influences the neurotransmitter and hypothalamic-pituitary-adrenal (HPA) axis. The main function of the HPA axis is to maintain homeostasis of various bodily processes, particularly the regulation of stress. One theory is that people undergoing ongoing stress may develop poorly regulated neuroendrocrine systems, so that exposure to even minor stress later on may cause the HPA axis to become reactive and result in difficulty returning to homeostatis.
Another hypothesis is that hormonal changes interact with the psychosocial. Role changes associated with reproductive events in societies that devalue women’s roles may result in depression. Although, in general, having positive peers is associated with less depression in adolescence (Gutman & Sameroff, 2004), for teen girls interpersonal stress may contribute to the onset of depression. Adolescent girls invest more than boys in relationships and tend to be more concerned about others’ approval in order to feel good about themselves (Girgus & Nolen-Hoeksema, 2006). These tendencies lead to greater sensitivity and reactivity to interpersonal stress (Rudolph, 2002), which may place them further at risk for relationship problems, which, in turn, results in distress. Social reasons for depression may involve the fact that the rate of sexual abuse is higher in females than in males (Barth, Bermetz, Heim, Trelle, & Tonia, 2013) and experiencing abuse leads to risk for depression. At the psychological level, girls may be more likely to use the coping strategy of rumination, which, as discussed, is problematic (Nolen-Hoeksema, 2002). When they are 12 years old, males and females diverge in their use of rumination, with girls showing higher rumination, and depression differences emerge about a year later (Jose & Brown, 2008).
The majority of adolescents with depression have received past-year treatment, but only a minority actually obtain treatment designed for depression or delivered from the mental health sector (Avenevoli et al., 2015). For this reason it is important for social workers to know the evidence basis for treatment. This section covers psychosocial treatment (psychotherapy) and medication, followed by studies that assess combining psychotherapy with medication.
Psychosocial treatment models that have been tested center on cognitive-behavioral treatment, interpersonal therapy, and family therapy.
Interventions based on cognitive-behavioral models include: (1) behavioral models that focus on the development of coping skills, especially in the domain of social skills and choosing pleasant daily activities, so that the youth receive more reinforcement from their environments, and (2) cognitive models that assess and change the distorted thinking that people with depression exhibit, in which they cast everyday experiences in a negative light. A few of the representative treatments are discussed here.
One representative treatment is The Adolescent Coping with Depression course (Clarke, Lewinsohn, & Hops, 1990), which includes the following components delivered over 15–16 sessions: (1) cognitive restructuring, (2) social skills training (how to make and maintain friendships), (3) communication and social problem solving (how to share feelings and resolve conflict without alienating others), (4) progressive relaxation training (to ease stress and tension), and (5) structuring mood-boosting activities into daily life. Some versions involve concurrent parent groups that involve sharing information about the topics and skills being taught in the adolescent group. The website has youth and practitioner manuals available, as well as a reference list of studies supporting the manuals.
Another example of cognitive-behavioral treatment is the Penn Prevention Program, also called the Penn Resiliency Program (Gillham & Reivich, 1999), which is a school-based group intervention for children ages 10–15. The two main components of the intervention are cognitive—cognitive restructuring and attribution retraining—and social problem solving—problem solving and teaching coping strategies for family conflict and other stressors. Weisz, Weersing, Valeri, and McCarty (1999) has developed another cognitive-behavioral treatment designed for youth ages 4 to 15 involving primary control (how to modify environmental conditions that are distressing) and secondary control (modifying subjective reactions to situations that cannot be changed).
Interpersonal therapy (IPT) is a brief (12-session), psychodynamic intervention focusing on how current interpersonal relationships have contributed to depression and helping teens repair these conflicts (Mufson, Dorta, Moreau, & Weissman, 2004). The general goals of IPT are to decrease depressive symptoms and to improve interpersonal functioning in the areas of role transitions, grief processes, and interpersonal disputes.
After presenting risk factors involving family factors as a rationale, Kaslow, Robbins Broth, Cowles Arnette, and Collins (2009) discussed various family-based interventions, including prevention and intervention, along with those that have a parental component for youth with depression. Although there are different types of treatment, including family psychoeducation, one representative family therapy model has been developed by Diamond, Diamond, and Levy (2013). It relies on attachment and family system theories as a basis and is designed to improve the quality of relationships in the family of the adolescent with depression.
Systematic Reviews on Treatment
The systematic reviews on the treatment studies offer important coverage of this literature. The most recent systematic review of the psychosocial treatment studies on depression with youth involved 52 studies and 3,805 patients (Zhou et al., 2015). After intervention, IPT and CBT but not psychodynamic therapy and play therapy were significantly more effective than control conditions. At follow-up, IPT and CBT were also significantly more effective than control conditions, although only IPT maintained this superiority at both short-term and long-term follow-up (6–12 months).
Nilsen, Eisemann, and Kvernmo (2013) conducted a literature review to examine pre-treatment child and adolescent characteristics as predictors and moderators of outcome in psychotherapy treatment trials of anxiety and depressive disorders. A literature search resulted in 13 depression studies. Non-significant associations between demographic factors (gender and age) with treatment outcome for the depression treatment trials were found. However, baseline symptom severity and comorbid anxiety was found to impact treatment response for youth with depression.
Antidepressants are currently being used by 3.2% of the U.S. adolescent population (Jonas, Gu, & Albertorio-Diaz, 2013). Tricyclic antidepressants (TCAs), so named because of their chemical structure, were the most commonly prescribed antidepressants through the 1980s. They work by blocking the reuptake of norepinephrine and serotonin and, to a lesser extent, dopamine (Bentley & Walsh, 2006). Although tricyclic medications have been studied in relation to depression, the available evidence is that they are not effective for children and show little benefit for adolescents (see Brown et al., 2007, for a review).
The newer antidepressants are characterized by their actions on serotonin. Selective serotonin reuptake inhibitor (SSRI) drugs block serotonin but in general do not interfere with the normal actions of norepinephrine. The dual serotonin and norepinephrine reuptake inhibitors (SNRIs) do not interfere with other chemicals affected by the Tricyclic antidepressants to cause adverse effects. Despite the rise in popularity in SSRIs and SNRIs, there are concerns about increased suicidal risk in youth taking antidepressants. Indeed, the United Kingdom has now banned SSRIs for youth 18 and younger, and in 2004 The U.S. Food and Drug Administration (2004) issued a “black box” warning label on SSRIs about this risk.
Systematic reviews of antidepressant treatment indicated that while SSRIs are more effective than TCAs (Qin et al., 2014), they are only more effective than placebo at a small effect and increase the risk of suicidal ideation by 58% (Hetrick, McKenzie, Cox, Simmons, & Merry, 2012). At this point, Prozac seems to be a first-line recommendation given the amount of research backing it for youth with depression (Bridge et al., 2007; Usala, Clavenna, Zuddas, & Bonati, 2008; Whittington et al., 2004). Zoloft has also received support for use in adolescents but not children.
Combining Psychosocial Treatment with Medication
Major studies on treatment of adolescents include the Treatment of Adolescents with Depression Study (TADS) and the Treatment of Resistant Depression in Adolescents study (TORDIA). These are covered here since they address the question of the differential effectiveness of psychotherapy and medication and their combination.
TADS is the largest treatment outcome study on adolescent depression (major depressive disorder) offered in multisites throughout the United States, with four randomized conditions: cognitive-behavioral therapy (CBT) alone for 12 weeks, fluoxetine (Prozac) alone, combining CBT and Prozac, and placebo. The CBT treatment offered was Weisz’s primary and secondary control described earlier. The TADS Team produced a report of the 36-week TADS follow-up (Weisz et al., 2006). Results at this point indicated Prozac seemed particularly effective for the treatment of depression; however, a concern was a greater risk of suicidality with medication. Although CBT did not produce as much improvement as medication, it sped up recovery when offered in combination. Offering CBT along with medication also seemed to protect against suicidal problems that emerged with treatment of Prozac.
Emslie et al. (2010) examined TORDIA involving 334 adolescents (ages 12–18) who had not responded to SSRIs and were then randomly assigned to either a medication switch alone (alternate SSRI or venlafaxine) or a medication switch plus CBT. At week 12, responders could continue in their assigned treatment arm and non-responders received open treatment (medication and/or CBT) for 12 more weeks (24 weeks total). Over one-third of participants (38.9%) achieved remission by 24 weeks, and initial treatment assignment did not affect rates of remission. Kennard et al. (2009) conducted a secondary analysis of the TORDIA study to explore the impact of specific CBT treatment components on outcome. Those who had more than nine CBT sessions were 2.5 times more likely to have adequate treatment response than those who had fewer than nine sessions. CBT participants who received problem-solving and social skills treatment were also more likely to have a positive response.
Cox et al. (2014) conducted a systematic review on the differential effects of medication and psychotherapy and their combination with children and adolescents diagnosed with depression. Although neither of these conditions emerged as more effective than the other, for treatment resistant-depression the combination of antidepressants and cognitive-behavioral therapy was effective for about half of the participants who had not responded to previous treatment (Zhou et al., 2014).
A systematic review of universal (primary) and targeted (secondary) prevention programs for depression was conducted (Werner-Seidler, Perry, & Calear, 2017), which can inform prevention efforts. A small effect size advantage was found for prevention programs, which, as the authors point out, can translate into significant impact. Targeted programs did better than universal programs, meaning that those targeting adolescents already at risk for depression were more effective than those that delivered the program to all students in the school.
There are logistical issues with screening for at risk status, however. Having all students complete a screening measure demands time and resources. There also may be possible stigma for those identified for services. Werner-Seidler et al. (2017) recommend that universal programs be implemented, followed by targeted interventions for those that do not initially respond to intervention. Note that some of the models described above, such as the Penn Prevention Program, Coping with Depression, and Interpersonal Therapy, have been used for prevention as well as treatment.
Depression is a serious problem that may first arise in adolescence, so those that work with teenagers should be aware of the signs and be able to screen and assess for symptoms in youth. This is particularly important in settings that interact with adolescents, such as child welfare and foster care, juvenile justice, and the school setting. Social workers should also be knowledgeable about the available treatments and make referrals and advocate to ensure that adolescents with depression receive optimal treatment.
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