Study Questions Ubiquinone’s Antioxidant Role, Industry Disputes Findings

09 Mar 2015 --- A study that questions co-enzyme ubiquinone’s traditional role as an antioxidant has been disputed by industry specialists. The research, carried out by McGill University, undercuts widely held belief that ubiquinone protects cells against damage from free radicals.

However, a leading international supplier of CoQ10, as it is widely known, says that the study is flawed. The study reveals that ubiquinone is not a crucial antioxidant -- and that consuming it is unlikely to provide any benefit.

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.
 
However, critics say that there are misleading statements about the study’s parameters. One leading supplier of co-enzyme Q10, and ubiquinol, its antioxidant form, as a nutraceutical ingredient with many properties, including anti-aging, told NutritionInsight: “We have to be mindful of how we interpret this article; without having seen the study itself, the title looks misleading at first sight.
 
“The study seems to mix effectiveness and the mechanisms by which the substance works or does not work, protection from oxidative stress in this case. This is always difficult to interpret without having seen the exact outcome measure,” said our industry source.
 
“The authors are also using ubiquinone, but we now use the antioxidant form of CoQ10, ubiquinol,” he continued. “Moreover, ubiquinol has significant higher bioavailability than ubiquinone, meaning that it will boost total CoQ10 levels to much higher amounts in blood plasma.
 
“CoQ10 and its active form ubiquinol, work in many different ways: cellular energy/ATP boosting, anti-oxidant protection and master gene regulation are some of the confirmed mechanisms. It is difficult to design a study that allows us to draw firm conclusions about presumed mechanisms,” he concluded.

The published research was supported by the Canadian Institutes of Health Research.

by Kelly Worgan
 
Full bibliographic information: "Mitochondrial function and lifespan of mice with controlled ubiquinone biosynthesis”, Ying Wang, Daniella Oxer & Siegfried Hekimi, Nature Communications, published online March 6, 2015. DOI: 10.1038/ncomms7393 http://www.nature.com/naturecommunications