Date of Award

Winter 1993

Project Type

Dissertation

Program or Major

Psychology

Degree Name

Doctor of Philosophy

First Advisor

Victor Benassi

Abstract

Abramson, Metalsky, and Alloy's (1989) theory of hopelessness depression is the most recent model of depression to emerge from the learned helplessness tradition (Seligman, 1975). Hopelessness theory describes an etiological pathway by which a unique subtype of depression--hopelessness depression--is believed to emerge.

The most proximal cause of hopelessness depression is the formation of a hopelessness expectancy. Experiencing a significant life stressor and either making stable and global causal attributions, anticipating adverse consequences, or inferring derogatory self-attributes is thought to contribute to hopelessness. In turn, generalized tendencies to make stable and global causal attributions, expect negative consequences, or perceive personal deficiencies in response to life stress purportedly increase the likelihood of making hopelessness-inducing inferences, and thus increase the risk of hopelessness and depressive symptoms.

The present research sought to (a) provide a comprehensive assessment of the proposed etiological pathway and (b) evaluate the competing predictions made by the hopelessness model and its most immediate theoretical precursor, the reformulated theory of learned helplessness depression (Abramson, Seligman, & Teasdale, 1978). In a two-wave panel design, college undergraduates $(N=247)$ completed measures assessing the constructs of both models. Higher levels of dysfunctional cognitive styles and event-based inferences predicted increases in depressive symptoms only among subjects who experienced an upsetting interpersonal stressor that was also perceived as uncontrollable. Little support was obtained for the hypothesis that hopelessness mediates associations between depressive symptoms and either maladaptive cognitive styles or event-inferences.

Consistent with the postulates of hopelessness theory, dysfunctional cognition appeared to render individuals vulnerable to depressive symptomatology in the face of life stress. However, the present findings call into question hopelessness theory's elimination of control perceptions in its etiological pathway. Continued study of the control construct is encouraged as are future tests of hopelessness theory that use more sophisticated assessments of life stress and fine-grained measures of hopelessness expectancies.

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