Coronary artery inflammation is reduced by coenzyme Q10

A study just published in the journal Nutrition offers welcome evidence that coenzyme Q10 reduces coronary artery inflammation. The authors state:

"The purpose of this study was to investigate the effects of coenzyme Q10 supplementation on inflammatory markers (high-sensitivity C-reactive protein [hs-CRP], interleukin-6 [IL-6], and homocysteine) in patients with coronary artery disease (CAD)."

In order to investigate the effects of coenzyme Q10 on coronary artery inflammation, they randomly assigned patients with coronary artery disease to a placebo group or one of two coenzyme Q10-supplemented groups (onethe Q10-60 group got 60 mg per day and the Q10-150 group got 150 mg/day) for 12 weeks. Then they measured plasma levels of coenzyme Q10, inflammatory markers (hs-CRP, IL-6, and homocysteine), malondialdehyde (a product of oxidative damage), and superoxide dismutase (antioxidant) activity. The higher dose of CoQ10 produced a significant reduction in the markers for coronary artery inflammation:

"The plasma coenzyme Q10 concentration increased significantly in the Q10-60 and Q10-150 groups. After 12 wk of intervention, the inflammatory marker IL-6 was decreased significantly in the Q10-150 group. Subjects in the Q10-150 group had significantly lower malondialdehyde levels and those in the Q10-60 and Q10-150 groups had greater superoxide dismutase activities. Plasma coenzyme Q10 was inversely correlated with hs-CRP and IL-6 at baseline. After supplementation, plasma coenzyme Q10 was significantly correlated with malondialdehyde and superoxide dismutase activities. However, there was no correlation between coenzyme Q10 and homocysteine."

It's interesting to note that it's not enough to show that plasma levels of CoQ10 go up—it's the functional result of reduced coronary artery inflammation that counts. IL-6 is an important pro-inflammatory cytokine that participates in coronary artery inflammation, hs-CRP is well-known. Oxidative stress as gauged by malondialdehyde and superoxide dismutase also participate in free radical oxidative reactions associated with vascular and other inflammation. The authors conclude:

"Coenzyme Q10 supplementation at a dosage of 150 mg appears to decrease the inflammatory marker IL-6 in patients with CAD."

When confronting the risk for or presence of vascular inflammation in general and coronary artery inflammation in particular, it is prudent to assess the patient's coenzyme Q10 status with the appropriate organic acid assay.

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