CoQ10 reduces key markers of inflammation, meta-analysis shows
- Meta-analysis of 17 randomized, placebo-controlled clinical trials
- Subjects include people with CVD, diabetes and other diseases
- CoQ10 dosage ranged from 60-300 mg/day, duration from 1 week to 4 months
- CoQ10 found to significantly reduce inflammatory markers (CRP, IL-6, TNF-alpha)
This meta-analysis was designed to evaluate the effect of co-enzyme Q10 (CoQ10) supplementation on inflammatory markers including C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha). Elevated levels of these pro-inflammatory markers increase chronic disease risk and contribute to disease pathogenesis.
Study inclusion criteria included randomized, placebo-controlled clinical trials with a parallel or crossover design lasting at least one week with outcome measures for CRP, IL-6 and TNF-alpha published in the peer-reviewed English-language literature from inception to August 1, 2016.
Seventeen studies (published from 2004 to 2016) met the inclusion criteria. Subjects include people with cardiovascular disease (CVD), diabetes, arthritis, multiple sclerosis, obesity, fatty liver disease, or renal disease. CoQ10 treatment ranged from 60 to 300 mg/day. Study duration ranged from one week to 4 months. No publication bias was found. Heterogeneity was found, but its influence was minimized by using a random-effects model and conducting subgroup and meta-regression analyses.
Based on the calculated weighted mean differences (WMD) with 95% confidence intervals, CoQ10 significantly (P<.03) reduced circulating levels of all three inflammatory markers: CRP (WMD: -0.35 mg/L), IL-6 (WMD: -1.61 pg/mL) and TNF-alpha (WMD: -0.49 pg/mL).
Meta-regression analysis showed the changes of CRP were independent of baseline CRP, treatment duration, dosage and patient characteristics. A higher baseline IL-6 level was significantly associated with greater effects of CoQ10 on IL-6 levels. A shorter treatment duration was significantly associated with greater effects on TNF-alpha, however, this result was based on a limited studies (n=2) and small weight, and therefore should be interpreted with caution.
The anti-inflammatory effect of CoQ10 is reported to be attributed, in part, to its ability to reduce nuclear factor kappa B (NF-kappa B)-dependent gene expression. NF-kappa B can be activated by reactive oxygen species and then up-regulates the expression of pro-inflammatory cytokines (such as TNF-alpha and IL-6). As an antioxidant, CoQ10 traps free radicals and inhibits the activation of NF-kappa B, which further inhibits the expression of pro-inflammatory cytokines.
These findings suggest that CoQ10 supplementation (60-300 mg/day) may offer clinical value in the treatment of chronic diseases in which inflammation plays a role, especially CVD and diabetes for which an elevated CRP level of is an independent risk factor.