TY - JOUR
T1 - The Job Demand-Control-Support Model and stress-related low-grade inflammatory responses among healthy employees
T2 - A longitudinal study
AU - Shirom, Arie
AU - Toker, Sharon
AU - Berliner, Shlomo
AU - Shapira, Itzhak
N1 - Funding Information:
The authors would like to acknowledge with thanks the financial support provided to the study by the Israel Science Foundation Grant 962/02·1.
PY - 2008/4
Y1 - 2008/4
N2 - We investigated the direct (additive) and interactive effects of the Job Demand-Control-Support (JDC-S) model's components on subsequent changes in three indicators of stress-induced low-grade inflammation in the body: C-reactive protein (CRP), fibrinogen and white blood cell count (WBC) plasma concentrations. These inflammation biomarkers have been shown to be implicated in the aetiology of cardiovascular disease. We studied separately healthy male (N=738) and female (N=383) employees who underwent periodic health examinations twice, about 18 months apart. Out of the 18 expected direct effects, only two, both supportive of our predictions, were found. Out of the 12 expected interactive effects derived from the JDC-S model, only two were found and both, when plotted on a graph, did not support the job strain model. We found no evidence supporting the possibility of reverse-causation, namely that each T1 fibrinogen, CRP and WBC predicted each T2 workload, control and support (controlling for their Time 1 values, respectively). We suggest that the physiological mechanism linking the JDC-S model with cardiovascular morbidity probably does not include inflammatory processes in the body.
AB - We investigated the direct (additive) and interactive effects of the Job Demand-Control-Support (JDC-S) model's components on subsequent changes in three indicators of stress-induced low-grade inflammation in the body: C-reactive protein (CRP), fibrinogen and white blood cell count (WBC) plasma concentrations. These inflammation biomarkers have been shown to be implicated in the aetiology of cardiovascular disease. We studied separately healthy male (N=738) and female (N=383) employees who underwent periodic health examinations twice, about 18 months apart. Out of the 18 expected direct effects, only two, both supportive of our predictions, were found. Out of the 12 expected interactive effects derived from the JDC-S model, only two were found and both, when plotted on a graph, did not support the job strain model. We found no evidence supporting the possibility of reverse-causation, namely that each T1 fibrinogen, CRP and WBC predicted each T2 workload, control and support (controlling for their Time 1 values, respectively). We suggest that the physiological mechanism linking the JDC-S model with cardiovascular morbidity probably does not include inflammatory processes in the body.
KW - C-reactive protein
KW - Fibrinogen
KW - Inflammation markers
KW - Job strain model
KW - White blood cell count
KW - Work-related stress
UR - http://www.scopus.com/inward/record.url?scp=46449095513&partnerID=8YFLogxK
U2 - 10.1080/02678370802180830
DO - 10.1080/02678370802180830
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???
AN - SCOPUS:46449095513
SN - 0267-8373
VL - 22
SP - 138
EP - 152
JO - Work and Stress
JF - Work and Stress
IS - 2
ER -