Major depressive disorder is common and costly, but not well understood. Even in light of the substantial literature on depression, some relatively basic questions remain unanswered, including, how exactly does depression develop and persist? Our lab at the University of Oregon, in collaboration with APS Fellow Ian Gotlib’s Stanford Mood and Anxiety Disorders Lab, has recently attempted to answer this question by employing a multi-method, longitudinal approach, guided by cognitive theory and state-of-the-art measures of life stress and cognitive vulnerability.
The Usual Suspects
A number of culprits have been implicated in the etiology of depression. They seemingly span all levels of analysis and include genetic, biological, physiological, cognitive, and social factors. Cognitive and social factors routinely have been considered primary suspects, kept in the lineup by theorists who have adopted a diathesis-stress perspective to explain depression onset. (The diathesis-stress model views psychological problems to be the result of stress affecting an individual who has a pre-existing vulnerability for developing a specific kind of problem.)
One of the most prominent diathesis-stress theories was developed by APS Fellow Aaron Beck, who proposed that depression onset may be attributed largely to negative cognitions and corresponding patterns of information processing. Beck’s model hypothesizes that individuals who experience adversity in childhood develop negative self-schemas that involve concepts like loss and inadequacy. These schemas are thought to remain dormant until an individual experiences a stressful life event that is reminiscent of the original stressor, at which point the schemas become activated.
When activated later in life, the schemas are believed to generate cognitions about the self, the world, and the future that are overly negative and extreme, such as “I am nothing if a person I love doesn’t love me.” Activated schemas are also thought to act as “filters” that guide the way in which events are perceived, evaluated, attended to, and remembered, leading to depressive affect that reinforces the activation of the negative schemas. Schemas are thus postulated to play an etiologic role in predisposing an individual to experience clinically-significant depression when the individual experiences stressful events that match, and thus activate, the negative schemas.
Researchers have examined predictions derived from Beck’s cognitive theory with mixed success. In particular, there now exists a large literature documenting the association of depression with dysfunctional attitudes and cognitive biases, but these findings are more consistent in demonstrating a connection between depression and concurrent cognitive dysfunction than in supporting the prediction that cognitive dysfunction precedes depression and that such cognitive biases are activated by stress.
The diathesis-stress predictions outlined in cognitive theory have not received more consistent support in part because multi-factorial research, comprising different levels of analysis, has rarely done justice to the many considerations unique to each level. This concern applies to the manner in which both life stress and cognitive vulnerability have been traditionally assessed: often via self-report measures in which the target construct and the disorder under study are blended.
Total (Automatic) Recall
We have attempted to address the need for better assessment by using investigator-based measures of life stress and computer-based measures of cognitive vulnerability. We assess life stress using the Life Events and Difficulties Schedule, which employs a semi-structured interview and a team of trained raters who make objective ratings of the reported events in terms of normative standards. The ratings obtained are based on the threat and unpleasantness of events, taking into account the individual’s unique biographical context.
We have chosen to measure cognitive vulnerability via methods borrowed from experimental cognitive psychology, including the Emotion Stroop task, the Emotion Face Dot-Probe task, and incidental free-recall and cued-recall memory tests. These tasks have permitted us to assess cognitive processes that are automatic, rather than strategic or controlled.
Our preliminary analyses have revealed that severe stressful life events occurring prior to depression onset are uniquely associated with elevated dysfunctional attitudes at onset, and that dysfunctional attitudes activated in this way abate with remission. We are currently analyzing the information processing data and expect parallel results.
Conducting multivariate research based on state-of-the-art methods is difficult, but certainly not impossible … and definitely preferable. The quality of our measurement should match the comprehensiveness of our theory, because anything less impedes progress toward better understanding precisely how depression develops and is maintained.
Film buffs will recognize that the subheadings in this article are movie titles. In keeping with that theme, I will close by saying that longitudinal empirical work, guided by theoretical insights and based on sound measurement, is our best bet and, perhaps, our only ticket to an entirely new film, titled “Diathesis-Stress Theories: The Next Generation.”
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