There is evidence for elevated levels of inflammatory markers in drug naïve depression when compared with general population. - GreenMedInfo Summary
Is Depression an Inflammatory Disease? Findings from a Cross-Sectional Study at a Tertiary Care Center.
Indian J Psychol Med. 2016 Mar-Apr;38(2):114-9. PMID: 27114622
Avin Muthuramalingam
BACKGROUND: Evidence linking inflammation and depression is marred by several methodological inconsistencies. Further, varying information is present on the role of gender as a potential confounder in this association.
AIMS: To assess systemic inflammation in drug naοve depression by measuring selected pro-inflammatory (tumor necrosis factor-alpha [TNF-α], interleukin-6 [IL-6]) and anti-inflammatory cytokines (transforming growth factor-beta [TGF-β]) and comparing them with a matched control group. We also aimed at exploring the differences in these markersbetween genders.
SETTING AND DESIGN: The study was a cross-sectional one carried out a teaching cum Tertiary Care Hospital.
MATERIALS AND METHODS: We recruited 55 drug naοve cases diagnosed with major depression and compared them for inflammatory markers with a matched apparently healthy control group (n = 42) at baseline. The inflammatory markers were also compared between the genders. Baseline depression and stress levels were assessed using standard measures.
STATISTICAL ANALYSIS USED: Mann-Whitney U-test.
RESULTS: In comparison with healthy controls, drug naοve depressed individuals demonstrated significantly raised baseline levels of TNF-α and IL-6 (P<0.001 for both) but no difference in levels of TGF-β (P = 0.433). Neither the baseline depression nor the stress scores correlated with any of the inflammatory markers (P = 0.955 and 0.816 for TNF-α respectively). Males and females were comparable on the levels of markers studied (P = 0.986, 0.415, and 0.430 for TNF-α, IL-6 and TGF-β respectively).
CONCLUSION: There is evidence for higher baseline inflammation in depression prior to starting anti-depressant therapy. Gender does not mediate this observed link between inflammation and depression.