Cognitive Vulnerability to Bipolar Spectrum Disorders

Lauren B. Alloy

Temple University

Noreen A. Reilly-Harrington

Harvard Medical School

David M. Fresco

Case Western Reserve University

Ellen Flannery-Schroeder University of Rhode Island

Until recently, the basis of the research and theories covering bipolar disorder has been almost exclusively biological in nature. Despite the pioneering work of Kraepelin (1921) suggesting that environmental factors play a part in precipitating manic and depressive episodes, conceptions of bipolar disorder as a genetically based biological illness have dominated over the past century—and rightfully so. The data from family, twin, and adoption studies suggesting that bipolar disorder carries a strong genetic predisposition (Goodwin & Jamison, 1990; Nurnberger & Gershon, 1992) and from pharmacotherapy trials indicating the effectiveness of lithium and anticonvulsive drugs in controlling the cycling of bipolar disorder (e.g., Keck & McElroy, 1996) are rather convincing (Miklowitz & Alloy, 1999).

However, there has been a growing interest in the role of psychosocial processes in the onset, course, and treatment of bipolar spectrum disorders. This resurgence of interest in psychological and environmental processes in bipolar disorder is largely attributable to four factors. First, although genetic and biochemical processes are undeniably important in the etiology, course, and treatment of bipolar disorder, they cannot fully account for differences in the expression of the disorder or the timing and frequency of symptoms (O'Connell, 1986). Second, there has been an in creased recognition of the limitations of prophylactic lithium usage. In fact, in a 1990 workshop report, the National Institute of Mental Health called for a further exploration of the impact of psychosocial factors on the course of bipolar disorder as well as the development of psychosocial treatments as an adjunct to pharmacotherapy (Prien & Potter, 1990). Third, there is growing evidence that stressful life events and negative family interactions influence the course of bipolar disorder (Johnson & Roberts, 1995; Miklowitz, Goldstein, & Nuechterlein, 1995). Finally, the huge success of cognitive models (e.g., Abramson, Metalsky, & Alloy, 1989; Beck, 1967, 1987) in understanding the etiology, course, and treatment of unipolar depression has led to the extension of these models to bipolar spectrum disorders with promising initial results (e.g., Alloy, Abramson, Walshaw, & Neeren, in press; Alloy, Reilly-Harrington, Fresco, Whitehouse, & Zechmeister, 1999; Hammen, Ellicott, & Gitlin, 1992; Reilly-Harrington, Alloy, Fresco, & Whitehouse, 1999).

Consequently, this chapter reviews recent theory and empirical research on the role of cognitive styles and life events as vulnerability factors for the onset and course of bipolar spectrum disorders. It begins by describing the nature of the bipolar spectrum. Then it presents the cognitive vulnerability-stress models of unipolar depression and the logic of their extension to bipolar spectrum disorders. Next, it discusses the methodological challenges posed by the group of bipolar disorders for vulnerability research. It covers the extant studies of life events and cognitive styles associated with bipolar disorders and predictive of bipolar symptoms and episodes. Finally, it looks at the implications of the current findings for the continued development of cognitive behavioral adjunctive treatments for bipolar disorders. The exploration of cognitive vulnerability-stress approaches to bipolar disorders is only at its beginning. Hopefully, spurred on by the current review, future investigators will conduct further, more sophisticated studies of the impact of cognition and stress on the onset and course of bipolar spectrum disorders.

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