Although exploratory, our study provides suggestive evidence for trauma’s potentially moderating influence on the effectiveness of a cognitive-behavioral intervention designed to prevent depression among urban, low-income mothers. On aggregate, PSE appeared to have a positive effect on preventing depression among our study population – close to half of which reported experiencing violent trauma in their lives. However, this impact appeared to be attenuated among the subpopulation with a history of trauma. Conversely, among the subpopulation without trauma history, PSE appeared to reduce the rate of clinically significant depressive symptomatology substantially, and even achieve statistical significance in some of our models.
Our findings are consistent with a growing body of literature demonstrating that major depression, in the presence of post-traumatic stress symptoms, can be more refractory to treatment than depressive disorder alone (Holtzheimer et al. 2005
). Our results are novel, however, because they suggest that the principle of intervention moderation extends to a risk prevention – as opposed to treatment – paradigm. Before an individual experiences a major depressive episode, antecedent risks are often present: sustained subsyndromal symptoms; poverty; or, in our case, the illness of a child. Similarly, before an individual develops post-traumatic stress symptoms or PTSD, she must experience an antecedent trauma. Our study, therefore, is an example of how antecedent risks to either depression or PTSD may interact to modify the success of a selective depression prevention strategy. To our knowledge, our study is the first to examine the impact of trauma – a common exposure among young urban women – on the ability to prevent depression.
Numerous recent reports on maternal depression’s high prevalence, as well as its adverse impact on children, have attempted to inform practice and policy debates. Facilitating and mandating reimbursement for maternal depression screening in clinical settings, furthermore, has been a centerpiece of many recent policy and legislative agendas (Earls 2010
; Illinois 2007
; New Jersey 2006
). Largely absent from this discussion, however, has been a focus on violence exposure, trauma, or post-traumatic stress, and how these coexistent risks may inform depression screening, treatment, or prevention practices. In a previous report, our group estimated that approximately one quarter of depressed urban mothers could have comorbid PTSD, and that over half report significant trauma exposure (Silverstein et al. 2010
). Our current report suggests that such exposure may have clinical ramifications relative to the ability to prevent depression.
This study has a number of limitations. First, it is exploratory; and in the context of our pilot work, we consider our finding to be more hypothesis-generating than confirmatory. Second, our study sample represents a combination of two distinct pilot trials; and it could be that our findings would not stand up if tested within a single, larger study. However, because our trials shared a common intervention, common measures, and a common study team, combining them is methodologically equivalent to conducting a single, stratified RCT. Third, although we obtained trauma histories from a valid and reliable PTSD instrument, we did not probe specifically for multiple traumas, timing of exposure, or recurrence. Although this lack of granularity in measuring trauma would most likely cause a conservative bias, it could be that certain traumas produce more substantial moderating effects than others. Fourth, we did not have enough subjects with high levels of PTSD symptoms to conduct an analysis of potential effect modification by PTSD symptom burden, or to assess whether the impact of trauma exposure is mediated through such symptomatology. Lastly, myriad other exposures, psychiatric comorbidities, ongoing life stressors, and concurrent treatments (medications or psychotherapy) could play clinically significant roles in modifying the effect of depression treatment and prevention programs; and it was beyond the scope of both our aims and sample size to test these influences.
These limitations not withstanding, our results lend credence to the hypothesis that trauma exposure may limit the effectiveness of certain depression prevention strategies. In future studies of depression prevention interventions – particularly among urban populations – investigators should give careful consideration to granular measurement of stressful life exposures and post-traumatic stress symptoms, and to measuring the moderating impact of such exposures and symptoms on intervention impact. If such a finding proves to be consistent, it may be that trauma-specific elements need to be incorporated into future prevention strategies.