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DEPRESSED PATIENTS HAVE ELEVATED C-REACTIVE PROTEIN INDEPENDENTLY OF GENETIC, HEALTH AND PSYCHOSOCIAL FACTORS, IN THE UK BIOBANK

Research output: Contribution to journalArticlepeer-review

Original languageEnglish
JournalThe American Journal of Psychiatry
Accepted/In press25 Nov 2021

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Abstract

ABSTRACT Objective: This project investigated the pathways leading to inflammation in major depressive disorder (MDD) – genetic, environmental, lifestyle, medical – using C-reactive protein (CRP), genetic, and phenotypic data of UK Biobank. Methods: This was a case-control study of 26,894 depressed participants with a lifetime MDD diagnosis from the Composite International Diagnostic Interview and 59,001 controls who reported no mental disorder and had not reported taking any antidepressant medication. Linear regression models of logCRP were fitted to regress out the effects of age, sex, body mass index (BMI) and smoking, and to test whether: (1) the polygenic risk score (PRS) for MDD was associated with logCRP; and (2) the association between logCRP and the MDD remained after adjusting for early life trauma (Childhood Trauma Screener), socio-economic status (Townsend Deprivation Index), and self-reported health status. Results: CRP levels were higher in depressed cases vs controls (2.4 vs 2.1 mg/L, p<10x10-10), and more cases than controls had CRP>3 mg/L (21.2 vs. 16.8%), indicating ‘low-grade’ inflammation. MDD PRS was positively associated with logCRP levels (beta=0.017, p=1.17x10- 6), but this association was no longer significant after adjustment for BMI and smoking. The association between MDD and increased logCRP was substantially reduced, but still remained significant, after adjustment for the aforementioned clinical and sociodemographic factors (fully adjusted model, beta=0.024, p=5.87x10-4). Conclusions: The data indicate that the ‘genetic’ contribution to the increased inflammation in depression is due to regulation of eating and smoking habits rather than an ‘autoimmune’ genetic predisposition. Moreover, the association between depression and increased inflammation even after full adjustment indicates either the presence of yet unknown/unmeasured psychosocial and clinical confounders, or that a ‘core’ biological association between depression and increased inflammation exists independently from confounders.

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