Cognitive Mechanisms Reciprocally Transmit Vulnerability between Depressive and Somatic Symptoms.

Kaitlin A. Harding,Karly M. Murphy,Amy Mezulis

doi:10.1155/2015/250594

Kaitlin A. Harding, Karly M. Murphy + Show 1 more

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https://doi.org/10.1155/2015/250594

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Abstract

Despite high comorbidity between depressive and somatic symptoms, cognitive mechanisms that transmit vulnerability between symptom clusters are largely unknown. Dampening, positive rumination, and brooding are three cognitive predictors of depression, with rumination theoretically indicated as a transdiagnostic vulnerability through amplifying and diminishing affect in response to events. Specifically, the excess negative affect and lack of positive affect characteristic of depressive symptoms and underlying somatic symptoms may cause and be caused by cognitive responses to events. Therefore, the current study examined whether comorbidity between depressive and somatic symptoms may be explained by the cognitive mechanisms of dampening and positive rumination in response to positive events and brooding in response to negative events among adults (N = 321) across eight weeks of assessment. We hypothesized that greater dampening and brooding would reciprocally predict greater depressive and somatic symptoms, while greater positive rumination would reciprocally predict fewer depressive and somatic symptoms. Mediation analyses in AMOS 22 indicated that dampening and brooding mediated reciprocal pathways between depressive and somatic symptoms, but positive rumination did not. Findings propose dampening and brooding as mechanisms of the reciprocal relationship between depressive and somatic symptoms through diminishing positive affect and amplifying negative affect in response to positive and negative events.

Highlights

Affective and somatic symptoms are common and debilitating categories of psychological health concerns in the United States, representing key causes of distress and impaired functioning across the lifespan
An international investigation of comorbid depressive and somatic symptoms across 15 countries determined that 30–62% of individuals with a Major Depressive Disorder diagnosis reported somatic symptoms that were not explained by a known physical etiology [7], which may be partially explained by the somatic nature of certain depressive symptoms
As a step toward integration, the current study examined the role of three cognitive mechanisms that may reciprocally explain the comorbidity between depressive and somatic symptom clusters using a multiwave study design

Summary

Introduction

Affective and somatic symptoms are common and debilitating categories of psychological health concerns in the United States, representing key causes of distress and impaired functioning across the lifespan. Somatic symptoms frequently cooccur with affective difficulties including anxiety, trauma-related, and depressive symptoms [1,2,3]. Of these comorbidities, cooccurring depressive and somatic symptoms may be of particular clinical and research concern. Research organizations including the World Health Organization describe both depressive and somatic symptoms as socially burdensome mental disorders globally and important focuses for research across nationalities and demographics [4,5,6]. Depressive and somatic symptoms are highly comorbid, with neither symptom category consistently preceding the onset of the other [8]

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