Work-Related Psychosocial Factors and Global Cognitive Function: Are Telomere Length and Low-Grade Inflammation Potential Mediators of This Association?

Abstract

The identification of modifiable factors that could maintain cognitive function is a public health priority. It is thought that some work-related psychosocial factors help developing cognitive reserve through high intellectual complexity. However, they also have well-known adverse health effects and are considered to be chronic psychosocial stressors. Indeed, these stressors could increase low-grade inflammation and promote oxidative stress associated with accelerated telomere shortening. Both low-grade inflammation and shorter telomeres have been associated with a cognitive decline. This study aimed to evaluate the total, direct, and indirect effects of work-related psychosocial factors on global cognitive function overall and by sex, through telomere length and an inflammatory index. A random sample of 2219 participants followed over 17 years was included in this study, with blood samples and data with cognitive function drawn from a longitudinal study of 9188 white-collar workers (51% female). Work-related psychosocial factors were evaluated according to the Demand-Control-Support and the Effort-Reward Imbalance (ERI) models. Global cognitive function was evaluated with the validated Montreal Cognitive Assessment (MoCA). Telomere length and inflammatory biomarkers were measured using standardised protocols. The direct and indirect effects were estimated using a novel mediation analysis method developed for multiple correlated mediators. Associations were observed between passive work or low job control, and shorter telomeres among females, and between low social support at work, ERI or iso-strain, and a higher inflammatory index among males. An association was observed with higher cognitive performance for longer telomeres, but not for the inflammatory index. Passive work overall, and low reward were associated with lower cognitive performance in males; whereas, high psychological demand in both males and females and high job strain in females were associated with a higher cognitive performance. However, none of these associations were mediated by telomere length or the inflammatory index. This study suggests that some work-related psychosocial factors could be associated with shorter telomeres and low-grade inflammation, but these associations do not explain the relationship between work-related psychosocial factors and global cognitive function. A better understanding of the biological pathways, by which these factors affect cognitive function, could guide future preventive strategies to maintain cognitive function and promote healthy aging.

Keywords: CRP; IL-6; cognitive function; demand–control–support; effort–reward imbalance; inflammatory biomarkers; mediation analysis; psychosocial stressors at work; telomere.

Figure 1

Flow chart of the study population.

Figure 2

Illustration of the total, direct, and indirect associations through telomere length and inflammatory index, between exposure to passive work and global cognitive function. M₀: Associations between exposure and mediators, or between mediators and global cognitive function. All associations were adjusted for age, sex, education, BMI, smoking, alcohol, physical activity, diabetes, hypertension, cardiovascular diseases, number of confidants, number of helpers, relationship with spouse, and relationship with children. Direct associations were additionally adjusted for inflammatory index, telomere length, inflammatory index squared, and interaction terms between telomere length and inflammatory index, and between telomere length and inflammatory index squared. Missing data on covariates, exposure, and outcomes were imputed with multiple imputation, and data were weighted for lost to follow-up between T1 and T2, and between T2 and T3, with an inverse probability of censoring weighting. * p < 0.05.