To our knowledge, this is the first study to demonstrate that OGM, in interaction with chronic interpersonal stress, predicts subsequent MDE onset in adolescents in remission from MDD or mDD. In our sample, as the proportion of specific memories decreased, the probability of MDE onset over follow-up increased for those who experienced higher levels of chronic interpersonal stress. Furthermore, our findings highlight that it is chronic interpersonal stress in particular that interacts with OGM in predicting the course of depression. When both chronic interpersonal and non-interpersonal stress were entered together, only chronic interpersonal stress predicted MDE onset in interaction with the proportion of specific memories. Although there was no significant main effect of chronic interpersonal stress, chronic non-interpersonal stress was a unique predictor of MDE onset over follow-up when it was entered along with chronic interpersonal stress. Specifically, the portion of chronic non-interpersonal stress that does not overlap with chronic interpersonal stress predicted MDE onset, with higher non-interpersonal stress levels associated with a lower probability of MDE onset over follow-up. This unexpected finding warrants replication but together these results suggest that interpersonal stress may play a more prominent role in increasing risk for depression in interaction with OGM than non-interpersonal stress.
Our findings are consistent with other studies examining the relationship between OGM, stress, and depression that have also found that the predictive relationship between OGM and higher levels of depressive symptoms at follow-up is greatest for individuals with high stress levels (Anderson et al., 2009
; Gibbs & Rude, 2004
). Furthermore, we extended this finding to a longer follow-up period than most research. Anderson et al. (2009)
and Gibbs and Rude (2004)
examined the relationship between stress, OGM, and the course of depression over 3 months and 4–6 weeks, respectively, whereas the current study followed participants over approximately 16 months. Spinhoven et al. (2006)
examined recurrence over a longer period (24 months), but they did not address the possible role of stress.
One difference between the current investigation and the studies by Anderson et al. (2009)
and Gibbs and Rude (2004)
is that in these prior studies, the stress measure covered the time between the AMT and follow-up assessment, whereas our measure of chronic stress covered the time surrounding the AMT. Nevertheless, this aspect of our design is in accordance with the notion that cognitive bias in individuals in remission from depression may be most predictive of depressive relapse when the bias is measured under conditions of stress or induced negative mood (e.g., Segal, Gemar, & Williams, 1999
). Our results are consistent with a model of depression that posits that cognitive biases may increase vulnerability to depression under certain conditions. One interpretation of our findings is that an underlying OGM bias in individuals in remission from depression may only exert an effect on depression when the bias was measured under conditions of high chronic interpersonal stress. Additionally, OGM has been associated with impaired social problem-solving (Williams et al., 2007
), and it is possible that OGM may keep people from dealing effectively with their interpersonal stressors, thereby contributing to depression. OGM may also potentially block the beneficial positive reinforcement that derives from specific positive events and that would normally serve to buffer against negative stressors, thereby increasing the negative impact of stress and contributing to depression vulnerability. Additional longitudinal research measuring OGM, problem-solving, stress, and depression at more frequent intervals is needed to directly test these hypotheses, but our study does provide preliminary support.
Our finding of a significant OGM by chronic interpersonal stress interaction is important because most prior research has not examined the roles of stress and OGM in predicting the course of depression. Furthermore, we are unaware of any study using an interview-based stress measure that compares the effects of chronic interpersonal and non-interpersonal stress. Future research should continue to examine how interpersonal stress and OGM may interact to contribute to the onset and maintenance of depression. Additional work investigating the mechanisms by which this may occur would also be important. Research delineating how risk for depression is conferred will be informative, especially because OGM could potentially be a proxy indicator of more pervasive cognitive processing difficulties, such as a lack of cognitive flexibility. Our study cannot directly address this issue, but it is of interest to examine this phenomenon in future studies. Another limitation is that we did not address whether OGM predicts initial vulnerability to depression. However, we plan to examine this question in the larger longitudinal study as more participants experience first onsets of depression.
In summary, our study suggests that OGM and chronic interpersonal stress interact to influence the course of depression in adolescents. OGM is already an important phenomenon for understanding the development and maintenance of depression (e.g., Williams et al., 2007
), and our results suggest that at least some of the effects of OGM are strongest at higher levels of stress.