Coenzyme Q10: Could it be the real deal?

Admit it: You were surprised a legitimate study came out in support of Coenzyme Q10 supplements. You probably looked away at first, nervous a colleague would notice your interest in something complimentary or alternative. It’s shocking, isn’t it? What if the purveyors of supplements are right about something?

Part of me so wants it to be true. Everyone likes to root for the underdog. Tell me you wouldn’t love to see the alternative medicine crew actually win a single skirmish against the lords of medicine.

A recent study has at least raised the possibility that Coenzyme Q10–an enzyme that med students learn about in the first semester of medical school, then promptly forget–may actually benefit patients with established heart disease. Alternative medicine people have promoted Co Q10 for years, but no regular doctor has listened.

My problem with supplements, vitamins and even certain medicines is that too often they are used as substitutes for healthy living. People who eat fruits and vegetables don’t need mega-vitamins; people who eat fish don’t need fish oil, and those who exercise, eat well and maintain a normal body weight rarely face the decision to take a blood pressure medicine. That’s common sense. Look no further than the healthy 90-year old Hoosier. You think he achieved that with supplements?

Then there is the issue of science. Study after study support the obvious: a healthy lifestyle lessens the need for pills and elixirs. Not one legitimate study has ever shown vitamins or supplements improve hard outcomes, like mortality.

The new Co Q10 Study:

A recent study (Q-SYMBIO) presented at the European Heart Failure Congress 2013 deserves attention. (Full coverage on theHeart.org) Researchers from Denmark (and throughout Europe) gave CoQ10 capsules three times a day to about 200 patients with advanced heart failure. A similar group of 200 heart failure patients received placebo. The 400-patient study was randomized, controlled, blinded and follow-up lasted two-years. The endpoint of the study was any major adverse cardiovascular events (MACE)–unplanned hospitalization for heart failure, cardiovascular death, need for urgent transplantation, and mechanical support. They also compared overall death rates.

The results were strikingly positive for CoQ10. Major adverse heart-related events occurred in 14% of those on CoQ10 versus 25% on placebo. This difference reached statistical significance (p = 0.003). All-cause mortality was 9% in the CoQ10 group versus 17% with placebo (p =0.01). In addition, CoQ10-treated patients had a significantly lower cardiovascular mortality and fewer adverse events.

The primary investigator Professor Mortensen said: “CoQ10 is the first new medication to improve survival in chronic heart failure and it should be added to standard therapy.”

CoQ10 background:

CoQ10 is an important biochemical involved in energy production in the mitochondria of cells. It’s also an antioxidant. Patients with heart failure have low levels of CoQ10. (Statin drugs are also known to reduce levels of CoQ10.) Although CoQ10 is found in food (red meat, plants, and fish), ingested amounts are insufficient to impact low levels in patients with heart failure.

The idea is that replacing CoQ10 will improve energy production in the cell. Since impaired heart muscle function is the root cause of many cases of heart failure, replacing CoQ10 may improve heart function. Unlike other heart medicines, which block normal cellular process, CoQ10 actually enhances normal processes. Preliminary studies have shown mixed results. No CoQ10 study has ever shown a difference in mortality.

My initial reaction to Q-SYMBIO:

My gut reaction to the trial was positive. I liked its simplicity. Give 200 sick patients a pill and give another 200 a placebo. Then count stuff that matters, like heart failure episodes and death. The results seem hard to fudge—a death is a death.

Plus, it’s biologically plausible. Heart failure is a disease of energy deficits. Patients with weak hearts are net negative on energy. This is why beta-blockers work while drugs called positive inotropes do not. We used to think it was a good idea to bathe a weak heart in a drug that made it contract more strongly. The problem is energy reserve; the weak heart would improve transiently but then would give out. (It’s like the end of a marathon. You don’t get to the finish by running faster in the last 6 miles, you get there by conserving energy.) Beta-blockers work in heart failure because they improve the energy conservation of diseased heart cells. (By the way, that theory was disruptive when it came out in the 1980s. People thought it was nuts to give a drug that made a weak heart contract less vigorously.)

CoQ10 fits the plausibility picture because it replaces a depleted chemical in the energy-generation process of a diseased heart. It could help turn the energy balance to the good. Maybe.

Many questions remain:

The main reason to be cautious about these early results is that they have yet to be published in a peer-reviewed journal. This was only a presentation. The chief investigator would not comment on any of the specifics until the study is published. This is notable because we must know the details. Were patients taking accepted medical regimens? How many patients were lost to follow-up? Baseline characteristics of the groups can impact the results significantly.

There are also issues of statistical significance. Small numbers of patients combined with low event rates have led some to suggest the study was underpowered to tell a real difference in outcomes. The differences could represent the play of chance.

The study had been ongoing for a decade. Why has it taken this long to publish a seemingly simple 2-year trial?

Then there is the old adage: if it looks too good to be true, it usually is.

Conclusions:

I look forward to the final publication of the trial. It needs to be vetted before we change practice. Right now, Coenzyme Q10 supplements for heart failure remain a viable theory.

That said though, even a skeptic would agree that this small study should prompt larger trials. If this theory pans out, it would be a very remarkable finding indeed.

If nothing else, it would validate the many hours that doctors (at least this one) spent memorizing the cell cycle in biochemistry class.

JMM