Abstract
BackgroundThe purpose of the present study was to examine the efficacy of targeting inflammation as a means of improving mood following spinal cord injury (SCI) and explore the potential mechanisms of action.MethodsThe study was a randomized, parallel-group, controlled, clinical trial (NCT02099890) whereby 20 participants with varying levels and severities of SCI were randomized (3:2) to either the treatment group, consisting of a 12-week anti-inflammatory diet, or control group. Outcome measures were assessed at baseline, 1 and 3 months, and consisted of CES-D scores of depression, markers of inflammation as assessed by various pro- and anti-inflammatory cytokines and several amino acids related to depression.ResultsA significant group × time interaction was found for CES-D (Center for Epidemiologic studies Depression Scale) score (p = 0.01), the TRP/LNAA (tryptophan/large neutral amino acid) ratio (p = 0.04), the composite score of pro-inflammatory cytokines (p = 0.04), IL-1β (interleukin-1 beta) (p = 0.04), and IFN-γ (interferon gamma) (p = 0.03). Pearson’s r correlation showed significance between the ∆IL-1β and both the ∆CES-D score (r = 0.740, p < 0.01) and the ∆KYN/TRP (kynurenine/tryptophan) ratio (r = 0.536, p = 0.02). The ∆KYN/TRP ratio was also significantly correlated with the ∆CES-D score (r = 0.586, p = 0.01). Mediation analysis showed that the relationship between the ∆KYN/TRP ratio and the ∆CES-D score was mediated by the ∆IL-1β. Subgroup analysis showed that participants with high CES-D scores had significantly higher concentrations of IL-1β, and all correlations were maintained or strengthened within this subgroup.ConclusionsOverall, the results demonstrated the effectiveness of targeting inflammation as a means of improving mood in SCI, with potential mechanisms relating to the reduction in IL-1β and improvements in levels of neuroactive compounds related to the kynurenine pathway. Due to the limited sample size, results should be interpreted with caution; however, they are worthy of further examination due to the potential impact of inflammation on depression.Trial registrationClinicalTrials.gov ID: NCT02099890.
Highlights
The purpose of the present study was to examine the efficacy of targeting inflammation as a means of improving mood following spinal cord injury (SCI) and explore the potential mechanisms of action
Individuals with major depressive disorder (MDD) are commonly reported to demonstrate immune dysfunction in the form of chronic inflammation, and likewise, individuals with chronic inflammatory disorders are more prone to MDD [1,2,3]
As evidence suggests that inflammation contributes to depression, and SCI is typically characterized by a state of chronic inflammation as well as a high prevalence of depression, it was hypothesized that reducing levels of inflammation in this population would result in both molecular changes and corresponding improvements in mood
Summary
The purpose of the present study was to examine the efficacy of targeting inflammation as a means of improving mood following spinal cord injury (SCI) and explore the potential mechanisms of action. Individuals with major depressive disorder (MDD) are commonly reported to demonstrate immune dysfunction in the form of chronic inflammation, and likewise, individuals with chronic inflammatory disorders are more prone to MDD [1,2,3] Such a state has been proposed to be a contributing factor to symptoms of depression due to the complex bidirectional communicatory pathways between various systems of the body. Pro-inflammatory cytokines such as IL-1β (interleukin-1 beta) and TNF-α (tumor necrosis factor alpha) can alter extra-cellular concentrations of serotonin (5-HT) by upregulating corresponding transporters (SERT) [7,8,9]. In this way, such pro-inflammatory cytokines have the ability to directly reduce 5-HT levels within the brain which are associated with symptoms of depression
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