Kynurenine pathway metabolites are increased in inflammatory depression and decrease with omega-3 treatment
Abstract
Activation of the kynurenine pathway (KP) with resulting accumulation of neuroactive metabolites may be a downstream pathophysiological mechanism of inflammatory depression. The aims of this study were to investigate KP metabolites in inflammatory depression compared to non-inflammatory depression and healthy controls, and whether these metabolites change with nutraceutical interventions with potential KP-modulating effects. We combined data from two antidepressant clinical trials: one with omega-3 polyunsaturated fatty acids (n-3 PUFAs) and one with a Limosilactobacillus reuteri probiotic supplement as the active intervention. Patients with Major Depressive Disorder (MDD) (n = 170) were stratified at baseline according to high-sensitivity C-reactive protein (hs-CRP) levels into an inflammatory (hs-CRP ≥1 mg/L, n = 127) and a non-inflammatory (hs-CRP <1 mg/L, n = 43) group. We also included 80 non-depressed healthy controls (HC). We investigated between-group differences in KP metabolites at baseline, treatment-associated changes in these biomarkers and how they relate to clinical response. At baseline, the inflammatory depression group had significantly elevated levels of quinolinic acid (QUIN) (p < 0.01), 3-hydroxykynurenine (3-HK) (p < 0.05), and kynurenine (p < 0.05) levels compared to both non-inflammatory depression and HCs. N-3 PUFAs, but not probiotics or placebo, significantly decreased QUIN (p < 0.05) and 3-HK (p < 0.05). Higher baseline levels and a larger…
How strong is the evidence?
Evidence Hub reads this as a cohort study, done in people. Its evidence level is 3 of 5 (Moderate · trial / cohort / secondary analysis). Trials without a large randomized design, cohorts and secondary analyses give moderate evidence. Reported size: 170 participants or records.
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