Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/65654
Citations
Scopus Web of Science® Altmetric
?
?
Type: Journal article
Title: Mediation and modification of the association between hopelessness, hostility and progression of carotid atherosclerosis
Author: Pollitt, R.
Daniel, M.
Kaufman, J.
Lynch, J.
Salonen, J.
Kaplan, G.
Citation: Journal of Behavioral Medicine, 2005; 28(1):53-64
Publisher: Kluwer Academic/plenum Publ
Issue Date: 2005
ISSN: 0160-7715
1573-3521
Statement of
Responsibility: 
Ricardo A. Pollitt, Mark Daniel, Jay S. Kaufman, John W. Lynch, Jukka T. Salonen, and George A. Kaplan
Abstract: Hopelessness and hostility are linked to progression of carotid atherosclerosis (PCA). The purpose of this study was to replicate such relations and to evaluate the role of biological pathways involving hyperactivation of the sympathetic nervous system (SNS) and the hypothalamic–pituitary–adrenocortical (HPA) axis. PCA was evaluated by 4-year change in three ultrasound measures of intima-media thickness (IMT) in 1027 men aged 42–60 years at baseline. Effect modification and mediation of relationships between psychosocial factors and PCA were examined for the measures systolic blood pressure (SBP), fibrinogen, and waist-to-hip ratio (WHR), levels of which are indicative of activity along these pathways. Hopelessness and hostility were associated with PCA. Fibrinogen mediated to a moderate extent the association between hopelessness and PCA. SBP significantly modified the relation between hostility and PCA in participants of moderate hostility. The above biological pathways are implicated in the mechanisms connecting hopelessness, hostility, and PCA.
Keywords: hopelessness
hostility
IMT
SBP
fibrinogen.
Rights: © 2005 Springer Science+Business Media, Inc.
DOI: 10.1007/s10865-005-2563-y
Published version: http://dx.doi.org/10.1007/s10865-005-2563-y
Appears in Collections:Aurora harvest
Public Health publications

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.