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SOCIAL NETWORKS AND INFLAMMATORY MARKERS IN THE FRAMINGHAM HEART STUDY

Published online by Cambridge University Press:  27 January 2006

ERIC B. LOUCKS
Affiliation:
Department of Society, Human Development & Health, Harvard School of Public Health, Boston, MA, USA
LISA M. SULLIVAN
Affiliation:
Department of Biostatistics, Boston University, Boston, MA, USA
RALPH B. D’AGOSTINO Sr
Affiliation:
Department of Mathematics, Boston University, Boston, MA, USA National Heart, Lung and Blood Institute’s Framingham Heart Study
MARTIN G. LARSON
Affiliation:
Department of Mathematics, Boston University, Boston, MA, USA National Heart, Lung and Blood Institute’s Framingham Heart Study
LISA F. BERKMAN
Affiliation:
Department of Society, Human Development & Health, Harvard School of Public Health, Boston, MA, USA
EMELIA J. BENJAMIN
Affiliation:
Department of Medicine and Preventive Medicine, Boston University, Boston, MA, USA National Heart, Lung and Blood Institute’s Framingham Heart Study

Abstract

Lack of social integration predicts coronary heart disease mortality in prospective studies; however, the biological pathways that may be responsible are poorly understood. The specific aims of this study were to examine whether social networks are associated with serum concentrations of the inflammatory markers interleukin-6 (IL-6), C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1) and monocyte chemoattractant protein-1 (MCP-1). Participants in the Framingham Study attending examinations from 1998 to 2001 (n=3267) were eligible for inclusion in the study. Social networks were assessed using the Berkman–Syme Social Network Index (SNI). Concentrations of IL-6, CRP, sICAM-1 and MCP-1 were measured in fasting serum samples. Multivariable linear regression analyses were used to assess the association of social networks with inflammatory markers adjusting for potential confounders including age, smoking, blood pressure, total:HDL cholesterol ratio, body mass index, lipid-lowering and antihypertensive medication, diabetes, cardiovascular disease, depression and socioeconomic status. Results found that the SNI was significantly inversely associated with IL-6 in men (p=0·03) after adjusting for potential confounders. In age-adjusted analyses, social networks also were significantly inversely associated with IL-6 for women (p=0·03) and were marginally to modestly associated with CRP and sICAM-1 for men (p=0·08 and 0·02, respectively), but these associations were not significant in the multivariate analyses. In conclusion, social networks were found to be inversely associated with interleukin-6 levels in men. The possibility that inflammatory markers may be potential mediators between social integration and coronary heart disease merits further investigation.

Type
Regular Articles
Copyright
2006 Cambridge University Press

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