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Job strain associated CRP is mediated by leisure time physical activity: results from the MONICA/KORA study
Rebecca Emeny1, Marie-Elena Lacruz, Jens Baumert
1Institute of Epidemiology II, Helmholtz Zentrum Muenchen, German Research Center for Environmental Health, 85764 Neuherberg, Germany.
Insights
Workplace psychological stress (job strain) is linked to inflammation. Physical activity may mediate this effect, suggesting both direct and indirect impacts on cardiac health.
Area of Science:
- Occupational health
- Psychoneuroimmunology
- Cardiovascular disease research
Background:
- Psychological stress at work is a known cardiac risk factor.
- The precise mechanisms, whether neuroimmune or behavioral, remain unclear.
- This study investigated job strain's association with inflammation and endothelial dysfunction markers.
Purpose of the Study:
- To examine the cross-sectional associations between job strain and serum biomarkers of inflammation and endothelial dysfunction.
- To explore the mediating role of psychosocial and cardiometabolic risk factors in job stress-related inflammation.
- To understand the pathways linking workplace stress to physiological health outcomes.
Main Methods:
- Karasek job strain index used to measure work stress in 951 participants.
- Serum biomarkers, including C-reactive protein (CRP), measured from non-fasting blood samples.
- Multivariate regression and mediation analyses (Sobel test) employed to assess associations and mediating effects.
Main Results:
- High job strain reported by 50.7% of participants, associated with adverse workplace conditions and lifestyle factors.
- Significant association found between job strain and CRP, even after adjusting for coronary heart disease risk factors.
- Physical activity adjustment abrogated the job strain-CRP association, indicating a mediating role (p=0.04).
Conclusions:
- Job strain demonstrates both direct and indirect effects on inflammation.
- Physical activity emerges as a significant mediator in the relationship between job strain and inflammation.
- Findings highlight the complex interplay between work stress, behavior, and cardiovascular health.
Background:
Psychological stress at work is considered a cardiac risk factor, yet whether it acts directly through neuroimmune processes, or indirectly by increasing behavioral risk factors, is uncertain. Cross-sectional associations between job strain and serum biomarkers of inflammation and endothelial dysfunction were investigated. Secondary analyses explored the role of psychosocial/cardiometabolic risk factors as mediators of job stress associated inflammation in healthy workers.
Methods:
Information on risk factors was obtained in standardized personal interviews of a subcohort of working participants in the MONICA/KORA population (n = 951). Work stress was measured by the Karasek job strain index. Biomarkers were measured from non-fasting venous blood. Multivariate regression analyses were used to examine the association of job strain with inflammatory biomarkers. Mediation analysis (Sobel test) was used to determine the effect of psychosocial risk factors on the association between job strain and C-reactive protein (CRP).
Results:
High job strain was reported by half (n = 482, 50.7%) of the study participants. While workers with high job strain were more likely to have adverse workplace conditions (competition with coworkers, job dissatisfaction and insecurity), sleeping problems, depressive symptoms, a Type A personality, and be physically inactive, no differences in cardiometabolic risk factors were detected. A strong and robust association between job strain and CRP was observed in age and sex adjusted models, as well as models adjusted for classic coronary heart disease risk factors (β = 0.39, p = 0.006 and β = 0.27, p = 0.03, respectively). Adjustment for physical activity abrogated this effect (β = 0.23, p = 0.07), and a mediating effect of physical activity on stress-associated inflammation was demonstrated (p = 0.04).
Conclusions:
The analyses provide evidence for both a direct and an indirect effect of job strain on inflammation.
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