Coenzyme Q10 likely ineffective, study finds

The popular dietary supplement ubiquinone, also known as Coenzyme Q10, is widely believed to function as an antioxidant, protecting cells against damage from free radicals. But a new study by scientists at McGill University finds that ubiquinone is not a crucial antioxidant — and that consuming it is unlikely to provide any benefit.

The findings, by a team led by Professor Siegfried Hekimi in McGill’s Department of Biology, are published today (March 6) in Nature Communications.

Ubiquinone is a lipid-like substance found naturally in all cells of the body. Cells need it to produce energy from nutrients and oxygen — a function performed by tiny structures, known as mitochondria, within cells. Because it was also thought to function as an antioxidant, ubiquinone has been recommended for a variety of ills and as an anti-aging supplement; global sales of the substance are estimated to amount to hundreds of millions of dollars a year.

“Our findings show that one of the major anti-aging antioxidant supplements used by people can’t possibly act as previously believed,” Hekimi says. “Dietary supplements cost a lot of money to patients throughout the world – money that would be better spent on healthy food. What’s more, the hope for a quick fix makes people less motivated to undertake appropriate lifestyle changes.”

In order to study how energy metabolism affects aging, the McGill researchers created the first strain of mice in which scientists are able to gradually eliminate ubiquinone — and then to restore it at will to normal levels. Because of ubiquinone’s role in energy production, loss of the substance in the mice led to severe sickness and early death. But the researchers were surprised to find no signs of elevated oxidative damage to cell membranes or DNA from free radicals, the sometimes-harmful molecules created by the oxygen chemistry during metabolism. The team also determined that this unexpected lack of damage didn’t stem from deployment of some other antioxidant strategies by the animals.

At the same time, the research yielded new insights into the importance of ubiquinone in helping mitochondria produce energy. “Many patients are sick because their mitochondria don’t work properly, including because they don’t contain enough ubiquinone,” Hekimi says. “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.” To that end, his research team recently received a grant from MitoCanada, a charity that seeks to help patients with mitochondrial diseases.

4 COMMENTS

  1. ScienceDaily quotes Danish Professor Mortensen as saying, regarding the results of the Q-SYMBIO study, “CoQ10 is the first medication to improve survival in chronic heart failure since ACE inhibitors and beta blockers more than a decade ago and should be added to standard heart failure therapy.” Those results were published at http://heartfailure.onlinejacc.org/article.aspx?articleid=1911013.
    To state, as does the headline here, that “CoQ is likely ineffective” is as absurd as stating that ATP is ineffective, or that epinephrine is ineffective. Ineffective at what? The headline is unscientifically vague. Your article states that “it is widely believed” that CoQ can “protect” cells against oxidative damage, although that supposed fact is undocumented, but, even if that were so, is that why people are taking it? No doubt there are many users of the substance who imagine that it will do things that it cannot. Yes, CoQ10 is ineffective at raising the dead, for instance, and I’m sure that some of its users have all kinds of ridiculous notions about what it does.
    Logic would suggest that the primary use of it has been by statin users who are totally unaware that there exist people who are taking it for its supposed “antioxidant” abilities; they most likely consume it because of statins’ well-demonstrated lowering of bodily CoQ10 levels, regardless of what they think that increasing those levels might do.
    “In apparent recognition of the significant adverse effects associated with statin-induced coQ10 depletion, two patents were awarded to Merck and Co. (now Merck, Sharp and Dohme) in 1990 for the combination of Mevacor in particular and statins in general with 1000 mg of coQ10. U.S. Patent No. 4,933,165 was issued for the following therapy: “A method of counteracting HMG-CoA reductase inhibitor-associated skeletal muscle myopathy in a subject in need of such treatment which comprises the adjunct administration of a therapeutically effective amount of HMG-CoA reductasc inhibitor and an effective amount of Coenzyme Q10 to counteract said myopathy.” Merck is also the assignee for U.S. Patent No. 4,929,437, which applies to pharmaceutical composition and method of counteracting elevated transaminase levels associated with HMG-CoA reductase inhibitor. The method described comprises the adjunct administration of an effective amount of a statin inhibitor and an effective amount of coQ10. These actions indicate that Merck was convinced of the clinical value and market potential of administering coQ10 in conjunction with statins, at least enough to apply for and receive patents for that combination of therapies.”–Herb, Nutrient, and Drug Interactions: Clinical Implications and Therapeutic Strategies, by Mitchell Bebel Stargrove, Jonathan Treasure, Dwight L. McKee. Elsevier, 2007.

  2. The author of this little piece ought to be fired. The article as written is biased and the title does not reflect but a portion of the research results.

    As @Chris said COQ10 actions are far broader than being merely an antioxidant. In fact Chris and Hops remarks are accurate.

  3. Given that mice died without CoQ10, it seems advisable to take it when taking statins, which lower CoQ10 production. If you take statins, which I wouldn’t….

  4. This study assumes that CoQ10 only acts as an antioxidant. CoQ10 is multi-functional. In fact it’s role as an antioxidant is minor at best compared to it’s other critical roles to health. As the study stated, the mice died shortly after the Ubiquinone was reduced. This is because every cell in the body is dependent on CoQ10 to create energy. Energy is essential to all biological functions. Therefore low intrinsic CoQ10 levels can lead to essentially every malady associated with low biological energy (ATP) production. I have to seriously question the authors of this article. Without proper context, this article is highly misleading. Plus, the authors suggest that only a proper meal can provide the necessary nutrients for proper health. While proper nutrition is crucial, there are a number of components necessary to optimal heath that are not found in enough abundance to meet biological requirements. The proper use of the right supplements can make all the difference in the world. Of Note: Ubiquinone is a precursor to Ubiquinol. 95% of Ubiquinone coq10 is converted to Ubiquinol CoQ10 in the body. For this reason Ubiquinol is known as active CoQ10. The study suggests that Ubiquinone was removed and no change to free radical breakdown was noticed. Is this because Ubiquinol remained? Again, I seriously question the authors of this article.

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