Ubiquinone, otherwise ubiquitously known as CoQ10, is one of the most popular dietary supplements, and is often taken for heart health and improving cardiovascular function. Now, a recent study has shed new light on how CoQ10 works, suggesting that its positive health effects may not be due to antioxidant activity. Published in Nature Communications, the study investigated mice whose CoQ10 levels researchers could manipulate. Researchers discovered that when they depleted mice of CoQ10, the level of oxidative damage to the mice cell membranes and DNA did not increase—this was surprising to researchers because they expected there to be more oxidative damage when CoQ10 was depleted if, in fact, CoQ10 was acting as an antioxidant. Another possible explanation for why there was not more oxidative damage was that CoQ10 was working to keep oxidative damage down, but another antioxidant took its place when it became depleted. Researchers, however, did not find any evidence for this explanation, and concluded that CoQ10 simply did not appear to function as an antioxidant. Nevertheless, there are a few important considerations to keep in mind when evaluating the findings of this study:
Even if future research confirms these results, this does not mean that taking CoQ10 doesn’t provide any health benefits. It simply means that how CoQ10 achieves these benefits is different than previously thought.
In fact, numerous double-blind trials have shown that CoQ10 may help improve, among other things, symptoms of angina; hypertension; and recovery from congestive heart failure.
Further, the researchers of the new study noted that restoring CoQ10 levels and mitochondrial function could help reverse certain disease states. The lead researcher of the study commented that “Many patients are sick because their mitochondria don’t work properly, including because they don’t contain enough ubiquinone. . . . We’ll be using the results of this study to devise ways, and possibly new drugs, to boost ubiquinone levels or help residual ubiquinone to function effectively in defective mitochondria.”
Source: Nature Communications