Journal
JOURNAL OF AFFECTIVE DISORDERS
Volume 150, Issue 3, Pages 736-744Publisher
ELSEVIER
DOI: 10.1016/j.jad.2013.06.004
Keywords
Inflammation; CRP; IL-6; Depressive; Longitudinal; Meta-analysis
Categories
Funding
- Medical Research Council (UK)
- Gordon Edward Small Charitable Trust
- Norman Collisson Foundation
- HDH Wills 1965 Charitable Trust
- National Institute for Health Research (England)
- OHSRC/BRC/NOF/OUCAGS
- Medical Research Council [G1001354] Funding Source: researchfish
- MRC [G1001354] Funding Source: UKRI
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Background: Inflammatory markers are raised in cross-sectional studies of depressed patients and may represent an important mediating factor for behaviour, neural plasticity and brain structure. Methods: We undertook a systematic review of longitudinal studies, investigating whether raised inflammatory markers indicate an increased risk of subsequent depressive symptoms. We searched three databases (1970-2012) for longitudinal studies with repeat data on CRP or IL-6 levels and subsequent depressive symptoms. We calculated effect sizes using a mixed-effects model, with separate meta-analyses for inflammatory markers and age groups. Results: We identified eight papers for CRP (14,832 participants) and three for IL-6 (3695 participants). There was a significant association between increased CRP and depressive symptoms (weighted-mean effect size 'unadjusted r'=0.069, p<0.0005; 'adjusted r'=0.046, p<0.0005), with moderate heterogeneity between studies (Q=11.21, p=0.08,I-2=46.5). For IL-6 the weighted-mean effect size was smaller ('unadjusted r'=0.045, p-value=0.007; 'adjusted r'=0.097, p-value=0.06). Limitations: The meta-analysis was based on a relatively small number of studies (particularly for IL-6) and only two inflammatory markers. There was moderate heterogeneity between studies and some evidence of publication bias. Conclusions: Raised inflammatory markers have a small but significant association with the subsequent development of depressive symptoms. This is a robust effect which remains significant after adjustment for age and a wide range of factors associated with risk for depression. Our results support the hypothesis that there is a causal pathway from inflammation to depression. (C) 2013 Elsevier B.V. All rights reserved.
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