Robin Lengton1, Mariëtte R. Boon1, Susanne Kuckuck1, Johanneke E. Oosterman1, BrendaW.J.H. Penninx2, Elisabeth F.C. van Rossum1
(1) Obesity Center CGG, Department of Internal Medicine, Division of Endocrinology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands. (2) Department of Psychiatry and Amsterdam Public Health, Amsterdam UMC, Vrije Universiteit, Amsterdam, The Netherlands.
Background:
Chronic stress is linked to cardiometabolic diseases through increased glucocorticoid exposure, but the extent to which daily life stress can influence glucocorticoid regulation and cardiometabolic health remains underexplored. Therefore, this study aimed to investigate these associations in the general population.
Methods:
In total, 870 participants were included from the Netherlands Study of Depression and Anxiety (NESDA) (64.7% female, median age=47.0 years) without diagnosis of psychiatric disorders in the last six months prior to participating in the study. Daily life stress was assessed using the Daily Hassles questionnaire (DHQ, range 0-60). Salivary cortisol was analyzed for 1-h awakening cortisol, diurnal slope and evening cortisol. Also a 0.5 mg dexamethasone suppression test was performed. Associations between DHQ scores, glucocorticoid measures, and cardiometabolic health were studied using logistic and linear regressions, adjusted for potential baseline confounders.
Results:
After multivariable adjustment, each 1-point increase in DHQ score was associated with 1.05-fold (95%CI 1.01;1.10) increased odds for cardiovascular disease (CVD), but not with diabetes, metabolic syndrome, or obesity. DHQ scores were not associated with the glucocorticoid measures. However, a 1-point increase in cortisol suppression ratio was associated with 1.21-fold (95%CI 1.05;1.40) increased CVD risk. No effect modification between daily hassles and cortisol suppression ratio on CVD risk was observed.
Conclusion:
Increased daily hassles and higher cortisol suppression ratios, indicating increased glucocorticoid sensitivity, were independently associated with increased CVD risk. The absence of interaction between these factors suggests they influence CVD risk through separate pathways. These findings highlight the need for further research to better understand stress mechanisms and identify “stress profiles” most at risk for developing cardiometabolic diseases.