PURIFIED NUTRITIONAL SUPPLEMENTS
COENZYME Q10
Coenzyme
Q10, also known as CoQ, CoQ10, and ubiquinone, is found in the mitochondria of
many organs, including the heart, kidney, liver, and skeletal muscle. After
ingestion, the reduced form of coenzyme Q10, ubiquinol, predominates in the
systemic circulation. Coenzyme Q10 is a potent antioxidant and may have a role
in maintaining healthy muscle function, although the clini-cal significance of
this effect is unknown. Reduced serum levels have been reported in Parkinson’s
disease.
In
early clinical trials, small but significant reductions in systolic and
diastolic blood pressure were reported after 8–10 weeks of coenzyme Q10
supplementation. The exact mechanism is unknown but, if correct, might be
related to the antioxidant and vasodilating properties of coenzyme Q10. In
three well-designed randomized, placebo-controlled trials, coenzyme Q10 was
reported to significantly lower systolic blood pressure and dia-stolic blood
pressure by 11 mm Hg and 7 mm Hg, respectively, as compared with no change in
the placebo groups. Whether coenzyme Q10 can be used to lower blood pressure
remains unclear. Since all three clinical trials have shown a benefit, it is
possible that publication bias may be present. Furthermore, an exaggerated
treatment effect may occur as adequate randomiza-tion, blinding, and concealment
of allocation have been ques-tioned for these studies.
Low
endogenous coenzyme Q10 levels have been associated with worse heart failure
outcomes, but this association is likely because low levels are a marker for
more advanced heart failure, rather than a predictor of disease. Despite these
findings, coenzyme Q10 is often advocated to improve heart muscle function in
patients with heart failure. According to the most recent meta-analysis,
coenzyme Q10 was shown to improve ejection fraction by 3.7% with a more
significant effect being observed in patients not receiving
angiotensin-converting enzyme inhibitors. It is unclear whether the
improvements in ejection fraction are appli-cable to all patients with heart
failure, as more research is required to assess the role of coenzyme Q10 in
heart failure and its impact on disease severity.
The effects of
coenzyme Q10 on coronary artery disease and chronic stable angina are modest
but appear promising. A theo-retical basis for such benefit could be metabolic
protection of the ischemic myocardium. Double-blind, placebo-controlled trials
have demonstrated that coenzyme Q10 supplementation improved a number of
clinical measures in patients with a history of acute myocardial infarction
(AMI). Improvements have been observed in lipoprotein a, high-density
lipoprotein cholesterol, exercise toler-ance, and time to development of
ischemic changes on the electro-cardiogram during stress tests. In addition,
very small reductions in cardiac deaths and rate of reinfarction in patients
with previous AMI have been reported (absolute risk reduction 1.5%).
Statins reduce
cholesterol by inhibiting the HMG-CoA reductase enzyme . This enzyme is also
required for synthe-sis of coenzyme Q10. Initiating statin therapy has been
shown to reduce endogenous coenzyme Q10 levels, which may block steps in muscle
cell energy generation, possibly leading to statin-related myopathy. It is
unknown whether a reduction in intramuscular coenzyme Q10 levels leads to
statin myopathy or if the myopathy causes cellular damage that reduces
intramuscular coenzyme Q10 levels. In one of the largest studies, when
rosuvastatin was used in patients with heart failure, there was no association
between statin-induced low coenzyme Q10 levels and a worse heart failure
outcome. Furthermore, the study found no observable difference in the incidence
of statin-induced myopathy regardless of endog-enous coenzyme Q10 levels. More
information is needed to deter-mine which patients with statin-related myopathy
might benefit most from coenzyme Q10 especially as it relates to the specific
statin, the dose, and the duration of therapy.
Coenzyme Q10 is well
tolerated, rarely leading to any adverse effects at doses as high as 3000 mg/d.
In clinical trials, gastrointes-tinal upset, including diarrhea, nausea,
heartburn, and anorexia, has been reported with an incidence of less than 1%.
Cases ofmaculopapular rash and thrombocytopenia have very rarely been observed.
Other rare adverse effects include irritability, dizziness, and headache.
Coenzyme Q10 shares a
structural similarity with vitamin K, and an interaction has been observed
between coenzyme Q10 and warfarin. Coenzyme Q10 supplements may decrease the
effects of warfarin therapy. This combination should be avoided or very
carefully monitored.
As a dietary
supplement, 30 mg of coenzyme Q10 is adequate to replace low endogenous levels.
For cardiac effects, typical dosages are 100–600 mg/d given in two or three
divided doses. These doses increase endogenous levels to 2–3 mcg/mL (normal for
healthy adults, 0.7–1 mcg/mL).
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