Introduction
In addition to the major risk factors for cardiovascular disease (i.e., smoking, elevations in cholesterol, elevated blood pressure, diabetes, and physical inactivity/obesity), a number of other factors have, on occasion, been shown to be more significant than the so-called major risk factors. In particular, high sensitivity C-reactive protein (hsCRP), a blood marker that reflects different degrees of inflammation, has been identified as an independent risk factor for heart disease. In fact, hsCRP levels have been shown to be a stronger predictor of cardiovascular events than cholesterol levels including LDL cholesterol.
Elevations in hsCRP are closely linked to a number of factors including insulin resistance, increased oxidative stress and/or lack of dietary antioxidants, and the intake of pro-inflammatory fatty acids such as saturated fats, arachidonic acid (found in meat and dairy), and trans-fatty acids as well as a reduced intake of mono-unsaturated fats and the long-chain omega-3 fatty acids found in cold-water fish and fish oil supplements.
Background Data
As significant as hsCRP has been as a marker of inflammation in atherosclerosis, another marker interleukin-6 (IL-6) may be found to be an even more sensitive indicator. IL is a pro-inflammatory cytokine that is secreted by macrophages and smooth muscle cells in the atherosclerotic plaque. The inflammation caused by these components of the plaque are thought to be one of the chief causes of the plaque becoming unstable leading to the formation of blood clots that could result in a heart attack, stroke, or pulmonary embolism. Hence, it is thought that blood levels of IL-6 may reflect inflammatory reactions within the lesions of atherosclerosis with more sensitivity than hs-CRP which reflects more systemic inflammation.
New Data
Since low levels of coenzyme Q10 are common in patients with cardiovascular disease, researchers sought to investigate the effects of CoQ10 supplementation on hs-CRP and IL-6. Fifty-one patients with coronary artery disease were randomly assigned to a placebo group or one of two coenzyme Q10-supplemented groups (60 mg/d, Q10-60 group; and 150 mg/d, Q10-150). The treatment period was 12 weeks.
The plasma CoQ10 concentration increased significantly in both the Q10-60 and Q10-150 groups, but only those at the 150 mg dosage showed significant reductions in IL-6. Specifically, CoQ10 supplementation lowered IL-6 levels by 14% indicating another possible reason to supplement CoQ10. CRP levels were inversely related to plasma CoQ10 levels at the beginning of the study, i.e., higher CoQ10 levels were associated with lower CRP levels, but supplementation failed to lower CRP levels in a significant fashion. A possible explanation for the lack of effect was that CRP levels were below 0.3 (considered ideal) in 67% of the patients. A major shortcoming of the study, was there was no subset analysis to determine the effect of CoQ10 on the 33% of the patients with elevated CRP.
The takeaway message is that CoQ10 was shown to exert an additional mechanism of benefit in patients with coronary artery disease that may prove to be of extreme significance.
Reference:
Lee BJ, Huang YC, Chen SJ, Lin PT. Effects of coenzyme Q10 supplementation on inflammatory markers (high-sensitivity C-reactive protein, interleukin-6, and homocysteine) in patients with coronary artery disease. Nutrition. 2012 Jul;28(7-8):767-72.
