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Mediation of the association between vascular risk factors and depressive symptoms by c-reactive protein: Longitudinal evidence from the UK Biobank

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Schaare,  Herma Lina       
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Villringer,  Arno       
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Blöchl,  Maria       
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Citation

Romankiewicz, L., Schaare, H. L., Nestler, S., Villringer, A., & Blöchl, M. (2022). Mediation of the association between vascular risk factors and depressive symptoms by c-reactive protein: Longitudinal evidence from the UK Biobank. PsyArXiv. doi:10.31234/osf.io/m8zv4.


Cite as: https://hdl.handle.net/21.11116/0000-000B-F3B5-6
Abstract
People with vascular risk factors (VRFs) are at higher risk for depressive symptoms. Given recent findings implicating low-grade systemic inflammation in both vascular and mental health, this study examined the extent to which the VRF–depressive symptom association might be mediated by low-grade systemic inflammation. To this end, we analysed longitudinal data of 9,034 participants from the UK Biobank (mean age = 56.54 years), who took part in three consecutive assessments over the course of about 8 years. Cumulative VRF burden at baseline was defined as the presence of 5 VRFs (hypertension, obesity, hypercholesterolemia, diabetes, and smoking). Low-grade systemic inflammation was assessed using serum-derived C-reactive protein (CRP) and depressive symptoms were measured using the Patient Health Questionnaire-9 (PHQ-9). We performed mediation models using longitudinal data and a path analytic framework, while controlling for age, gender, racial-ethnic background, socioeconomic status, and baseline mood. VRFs at baseline showed a small association with higher depressive symptoms at follow-up (total effect = 0.014, 95% CI [0.007; 0.021]). CRP mediated this association (indirect effect = 0.003, 95% CI [0.001; 0.005]) and accounted for 20.10% of the total effect of VRF burden on depressive symptoms. Exploratory analyses taking a symptom-based approach revealed that mediating pathways pertained to specific depressive symptoms: tiredness and changes in appetite. These results suggest that the small association between VRF burden and depressive symptoms may be partly explained by the inflammation-promoting effects of VRFs, which might promote a specific symptom-profile of depression.