by Joye C. Anestis
In clinical psychology, we most often deal with healing mental disorders after they have reared their ugly heads. The majority of interventions written about on PBB target full-blown mental illnesses, as do the therapies considered to be empirically-supported treatments (ESTs). However, many researchers focus their energy on the other side of the disorder spectrum and are working to develop preventative treatments for individuals known to be at high-risk for developing a specific mental illness (e.g., people with significant genetic risk). Certainly, some would argue that developing ways to prevent mental illness should be the primary imperative for the clinical psychology (& other mental health) field.
Much of the prevention literature targets children and adolescents who are at high risk for eventually developing a mental disorder. The method of defining high risk individuals depends on the mental illness being studied, but familial risk is probably the most common indicator. Children and adolescents with a parental history of certain mental illness (e.g., depression, bipolar disorder, schizophrenia) are at a higher risk of developing that disorder. The study at hand (Garber et al., 2009, recently published in JAMA) focused on preventing depression in a sample of adolescents with a parental history of depression. In 2001, Clark and colleagues reported that a group cognitive-behavioral (CB) prevention program was more effective than usual care for the prevention of depression in adolescents whose parents had a history of depression. Garber et al. (2009) attempted to replicate these findings, hypothesizing that those in the CB program would have a lower incidence of depressive episodes and show a better outcome on continuous measures of depressive symptomatology. They also investigated whether other factors, such as current parental depression, current participant depression, and participant history of a mood disorder, moderated the effect of the intervention.
The sample: As is common in randomized controlled trials, individuals had to meet detailed exclusion criteria in order to participate in the study. Adolescents had to have at least 1 parent/caretaker who had a major depressive in the past 3 years, or 3+ episodes or 3+ cumulative years in a major depressive or dysthymic episode in the adolescent's lifetime. Additionally, the adolescents had to be 13-17 years old and have current subsyndromal depressive symptoms, a prior depressive episode that was in remission for at least 2 months, or both. Adolescents were also excluded if they had a current mood disorder diagnosis, were currently taking an antidepressant, had received more than 8 sessions of CBT for depression, or had a biological parent with bipolar I disorder or schizophrenia. Siblings could be included, and the randomization protocol ensured that siblings were assigned to the same condition. In all, 316 adolescents (58.5% female) participated, spread across 4 study sites (Nashville, Pittsburgh, Portland, and Boston).
The intervention: Participants were randomly assigned to either the treatment group or a control group, but the randomization procedure ensured that the 2 groups were equivalent on age, sex, race-ethnicity, and inclusion criteria. The treatment group (n = 159) received the CB preventative intervention. It consisted of 8 weekly 90-minute sessions (the acute phase) and 6 monthly sessions (the continuation phase) in mixed-sex groups of 3-10 adolescents. During the acute intervention, the participants were taught cognitive restructuring skills to identify and refute unrealistic and negative thoughts, as well as problem-solving skills. During the continuation sessions, cognitive restructuring and problems-solving were reviewed and some new skills were taught (e.g., relaxation, behavioral activation). At weeks 1 and 8 of the acute sessions, the parents attended the sessions to learn the general topics and skills being covered, as well as the rationale behind them. For the usual care control condition, all enrollees, regardless of randomized condition, were allowed to begin or continue nonstudy mental health or other health care service. Such service use was documented. Assessments of parents and adolescents were conducted before the intervention, immediately after the intervention (month 3), and after the continuation phase (9 months after baseline).
The results: Overall, the prevention programs worked. The treatment group developed new depressive episodes at a significantly lower rate than the control group,and self-reported depressive symptoms declined at a significantly greater rate for those in the CB program. Next, the investigators examined several factors to see if they moderated the effect of the treatment. Interesting, current parental depression significantly moderated the effect of the prevention program, meaning that the prevention program was significantly better at preventing a depressive episode if a parent was not currently depressed. When a parent was currently depressed, rates of incident depression (i.e., new episodes) in the youths did not significantly differ between the 2 groups. Within the prevention group, those whose parents were currently depressed had a significantly higher rate of incident depression than those whose parents were not currently depressed. This difference did not exist in the control group. The adolescents' own depressive history and depressive symptoms did not impact the outcome.
This study by Garber et al. builds on the literature showing the group CB intervention are effective in preventing the development of depression in adolescents who are at high risk for the disorder. Not only is this an important finding on the utility of CB techniques in holding a pernicious illness at bay, but adds to the growing literature supporting certain group treatments. Group treatments are more cost-effective for clients and are highly attractive to managed care companies, making it imperative for researchers to develop and examine the efficacy of these programs. An important caveat to Garber et al.'s overall results is the finding that the prevention program is most effective when their participants' parents are not currently depressed. This finding is consistent with previous findings showing a relationship between parental symptom improvement and child functioning (Gunlicks & Weissman, 2008). Garber et al. suggest that future studies should examine a combined or sequential parent and adolescent treatment/prevention program, an initiative that would be fascinating and possibly very helpful. On a pragmatic note, I imagine that such a program would be more cost-effective (certainly more so than waiting until the adolescent has been struggling with depression for many years). Additionally, I wonder if incorporating a child into the parental treatment would also be highly motivating for the parent, thus perhaps increasing the efficacy of CBT for depression. I would be very interested to read about that study.
Joye Anestis is a doctoral candidate in clinical psychology at Florida State University.



