TY - JOUR

T1 - Does inflammation provide a link between psychosocial work characteristics and diabetes?

T2 - Analysis of the role of interleukin-6 and C-reactive protein in the Whitehall II cohort study

AU - Magnusson Hanson, Linda L

AU - Virtanen, Marianna

AU - Rod, Naja H.

AU - Steptoe, Andrew

AU - Head, Jenny

AU - Batty, G. D.

AU - Kivimäki, Mika

AU - Westerlund, Hugo

N1 - Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.

PY - 2019

Y1 - 2019

N2 - OBJECTIVE: Inflammation may underlie the association between psychological stress and cardiometabolic diseases, but this proposition has not been tested longitudinally. We investigated whether the circulating inflammatory markers interleukin-6 (IL-6) and C-reactive protein (CRP) mediate the relationship between psychosocial work characteristics and diabetes.METHODS: We used three phases of data at 5 years intervals from the Whitehall II cohort study, originally recruiting 10,308 civil service employees aged 35-55 years. The data included repeat self-reports of job demands, control and social support, IL-6 from plasma samples, CRP from serum samples, and diabetes, ascertained through oral glucose tolerance test, medications, and self-reports of doctor-diagnosed diabetes.RESULTS: Structural equation models with age, sex and occupational position considering men and women combined, showed that low social support at work, but not high job demands or low job control, was prospectively associated with diabetes (standardized ß  =  0.05, 95% confidence interval (CI) 0.01-0.09) and higher levels of IL-6 (ß  =  0.03, CI 0.00-0.06). The inflammatory markers and diabetes were bidirectionally associated over time. A mediation model including workplace social support, IL-6 and diabetes further showed that 10% of the association between social support and diabetes over the three repeat examinations (total effect ß  =  0.08, CI 0.01-0.15) was attributable to a weak indirect effect through IL-6 (ß  =  0.01, CI 0.00-0.02). A similar indirect effect was observed for CRP in men only, while job control was prospectively associated with IL-6 among women.CONCLUSIONS: This study indicates an association between poor workplace support and diabetes that is partially ascribed to an inflammatory response.

AB - OBJECTIVE: Inflammation may underlie the association between psychological stress and cardiometabolic diseases, but this proposition has not been tested longitudinally. We investigated whether the circulating inflammatory markers interleukin-6 (IL-6) and C-reactive protein (CRP) mediate the relationship between psychosocial work characteristics and diabetes.METHODS: We used three phases of data at 5 years intervals from the Whitehall II cohort study, originally recruiting 10,308 civil service employees aged 35-55 years. The data included repeat self-reports of job demands, control and social support, IL-6 from plasma samples, CRP from serum samples, and diabetes, ascertained through oral glucose tolerance test, medications, and self-reports of doctor-diagnosed diabetes.RESULTS: Structural equation models with age, sex and occupational position considering men and women combined, showed that low social support at work, but not high job demands or low job control, was prospectively associated with diabetes (standardized ß  =  0.05, 95% confidence interval (CI) 0.01-0.09) and higher levels of IL-6 (ß  =  0.03, CI 0.00-0.06). The inflammatory markers and diabetes were bidirectionally associated over time. A mediation model including workplace social support, IL-6 and diabetes further showed that 10% of the association between social support and diabetes over the three repeat examinations (total effect ß  =  0.08, CI 0.01-0.15) was attributable to a weak indirect effect through IL-6 (ß  =  0.01, CI 0.00-0.02). A similar indirect effect was observed for CRP in men only, while job control was prospectively associated with IL-6 among women.CONCLUSIONS: This study indicates an association between poor workplace support and diabetes that is partially ascribed to an inflammatory response.

U2 - 10.1016/j.bbi.2019.01.017

DO - 10.1016/j.bbi.2019.01.017

M3 - Journal article

C2 - 30684651

VL - 78

SP - 153

EP - 160

JO - Brain, Behavior, and Immunity

JF - Brain, Behavior, and Immunity

SN - 0889-1591

ER -