Depressive rumination is defined as repetitive thinking about the causes, symptoms, and meaning of one's depressed mood. Rumination is associated with serious negative consequences, such as more severe, longer- lasting, and more numerous episodes of major depression. To understand why some individuals engage in such maladaptive thinking, previous research has attempted to elucidate cognitive mechanisms that may underlie rumination. Findings from this research suggest that inhibitory deficits make it difficult for ruminators to remove from working memory (WM) information that is no longer relevant and to exert cognitive control to keep irrelevant information from entering WM. Although this research has been successful in identifying cognitive aspects of rumination, little work has been conducted elucidating the neural mechanisms that underlie rumination. Identifying the neural underpinnings of rumination has the potential to increase our understanding of the mechanisms that drive this process. In this context, the overarching goal of the proposed research plan is to elucidate the neural mechanisms of depressive rumination.
One aim of this research is to use fMRI to identify brain regions associated with ongoing ruminations and to identify the neural mechanisms by which ongoing ruminations impair individuals'ability to control their attention.
A second aim of this research is to use fMRI and behavioral studies to examine the neural mechanisms that underlie the cognitive deficits that characterize individuals with a high tendency to ruminate. These studies will help to elucidate the neural mechanisms that may make it difficult for ruminators to control the contents of their WM. We will distinguish neural mechanisms that may precede and underlie a tendency to ruminate from mechanisms that may be a consequence of depressive rumination.

Public Health Relevance

. Elucidating the neural mechanisms that underlie and motivate rumination can benefit mental health research by leading to new ways for cognitive and pharmacological therapy to target more effectively the causes of this maladaptive thinking style. Such findings could help in both the prevention and the alleviation of clinical disorders. Moreover, if we can determine the neural signature of depressive rumination, we can use this information in future studies to test the effectiveness of new interventions aimed at reducing rumination, and to compare the neural bases of rumination to foundations of other forms of maladaptive thinking and behavior.

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32MH087115-03
Application #
8277425
Study Section
Special Emphasis Panel (ZRG1-F12B-S (20))
Program Officer
Rubio, Mercedes
Project Start
2010-07-01
Project End
2013-06-30
Budget Start
2012-07-01
Budget End
2013-06-30
Support Year
3
Fiscal Year
2012
Total Cost
$52,190
Indirect Cost
Name
Stanford University
Department
Psychology
Type
Schools of Arts and Sciences
DUNS #
009214214
City
Stanford
State
CA
Country
United States
Zip Code
94305
Whitmer, Anson J; Gotlib, Ian H (2013) An attentional scope model of rumination. Psychol Bull 139:1036-61
Whitmer, Anson J; Gotlib, Ian H (2012) Depressive rumination and the C957T polymorphism of the DRD2 gene. Cogn Affect Behav Neurosci 12:741-7
Whitmer, Anson J; Frank, Michael J; Gotlib, Ian H (2012) Sensitivity to reward and punishment in major depressive disorder: effects of rumination and of single versus multiple experiences. Cogn Emot 26:1475-85
Whitmer, Anson J; Gotlib, Ian H (2012) Switching and backward inhibition in major depressive disorder: the role of rumination. J Abnorm Psychol 121:570-8