General Cardiology Healthy Living Nutrition

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 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.


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.


24 replies on “Coenzyme Q10: Could it be the real deal?”

I remember hearing Dr. Julian Whittaker talk about CoQ10 over 20 years ago. A quick Google shows he still is ( ). This is not to say pro or con – but rather to offer perspective on how long this debate has been ongoing. Reservations raised on site (and by you above) about this non-published study are valid – and even when (if) published – for “proof”, results would have to be replicated. This may or may not eventually happen. So questions will remain and practice will probably not yet be changed.

On the other side – one main question is, “What harm?” from taking CoQ10? Bottom Line: Hard to know a definitive answer regarding ‘yay’ or ‘nay’ for CoQ10 without convincing evidence …

Thanks for the link KG. As for harm, I agree; the supplement has been around a long time and people seem to be tolerating it well. But on the other hand, as you say, without data, we just do not know. Perhaps these results will be enough to stimulate some interest in doing larger studies.

Two questions. (1) What is a reasonable dose of Coenzyme Q10? (2) Does Coenzyme Q10 help with statin intolerance (myalgia)?

Some reservations… a 400-patient study is not all that large. Second, in the 1980s, reducing myocardial oxygen demand was very much in vogue which made beta blockers a good choice. It was not such an unreasonable premise back then and it still works today. Who (or what company) financed the study? That means a lot in this day of “let’s publish the good results and bury the bad ones.”

I understand it wasn’t within the scope of the study, but would you believe/theorize that Q10 would provide any benefit to AF sufferers?

Some of the herbs that Mayo claims to be interaction risks have been debunked by pharmacokinetic studies. I wonder if this is another one of those warnings that’s based on a “case report” (i.e. anecdote) or in vitro assay. Intuitively, it just seems fishy. If supplementing up to a normal coQ10 level causes some kind of problem with warfarin, what about all those people who naturally have a normal coQ10 level?

It’s amazing how fast “p < .01" turns into "play of chance" when the result conflicts with the speaker's ideology.

Are you aware of the relationship of CoQ10 and another family of quinones: the menaquinones? There is increasing (and supportable) data that shows how essential menaquinones – vitamin K2 – is to heart health.
When statins are taken, not only CoQ10 biosynthesis is impaired, so is menaquinone biosynthesis of the form MK-4.
They all share UBIAD1 (also called TERE1) in their biosynthesis in the mevalonate pathway, thus statins contribute to bad heart health. Ironic.
Additionally, so do bisphosphonates impair menaquinone-4 biosynthesis.
Since matrix gla protein, the most potent anti-calcification molecule known, must have enough MK-4 (and other forms of vitamin K work with this form, such as long chain menaquinones) to prevent calcification in arteries, this looks to be a powerful method of optimizing heart health.
This finding is supported by understanding the pharmocokenetics of menaquinones and also by the cultures who have the longest and best health.
ALL cardiologists need to learn more about menaquinones.
There is no Rx drug…it is a missing and blocked nutrient that needs attention and most cardiologists are in the dark.
And, no, if you still believe that the vitamin K2 made by gut bacteria are contributing to OUR K status, they are not. They make this for themselves and we do not absorb any since absorption requires bile salts, which are not present in the lower gut where these bacteria live.
Almost EVERY single American is vitamin K deficient. Subclinically, but still deficient. With age, this rears up and is possibly totally treatable with more long chain menaquinones.

I’m wildly speculating here, but I do a lot of reading and enjoy piecing together information that seems to relate.

From what I’ve read, it’s fairly well accepted that statins do cause a loss of serum CoQ10.

Low levels of CoQ10 can cause a wide variety of problems, as it is important for proper functioning of muscles, brain and the retina (for starters). Some studies have shown that persons with AMD have low concentrations of CoQ10 in their retinal tissue. How that is determined, I don’t know. Perhaps with postmortem exams, or with animal retinal tissue experiments.

Could it be that the recent rise of dementia and AMD in the elderly is linked to the widespread use of statins in the past 15-20 years? If so, then it would be extremely important to investigate co-administration of CoQ10 with statin use.

Some of us have quite a mix of side effects from statins, so if CoQ10 could help relieve those side effects, it could be a win-win situation – the benefits of statins combined with the benefits of CoQ10.

Our body systems are such a complex maze of interactions.

Again, I’m just speculating from a average Joe perspective. As a technician in another field, I’m naturally curious about connecting bits of information to solve puzzles and problems.

More than a few of us have side effects from statins, but it would be great if supplementation with CoQ 10 truly helped and wasn’t adversely ruled by taking Warfarin.

Carol, I remember years ago looking in a Merck drug reference to bone up on the meds my parents were taking. They were not on Warfarin, but in looking over drug lists, it seemed every damn thing in the world was contra-indicated with Warfarin. I had no idea at the time what it was used for, but it struck me how perfectly awful and dangerous a drug it must be.

Now, looking at the dietary restrictions, and the vast list of prescription and OTC drugs you have to watch out for it’s a wonder people ever can keep it straight and in the safety zone. No wonder so much monitoring of INR is necessary.

I’d be really curious as to what the interaction is – does it increase or decrease the anti-coagulant action, or is it something else?

I’ve lived through years of seeing “miracle supplements” crash and burn after the initial hype, so I hope this doesn’t follow the same path. Some, however, have been proven over time, both in clinical trials, and in the real world, to actually work “as seen on TV”.

I know from my brief experiences with CoQ10, my overall being felt improved – both mental functioning as well as exercise tolerance, but that could have been irrational exuberance – who knows.

I don’t know about other people, but for me being on Warfarin: when I eat something that the medication interacts with, it comes across as a powerful nauseousness that sweeps through my stomach about 4 hours or so later and remains until I have tea and a snack. I sure don’t like feeling sick. Yogurt is an especially a bad choice for me. I felt nauseated most of last summer, and didn’t realize that the cause was the yogurt I put on my cereal. Spinach and other greens more than likely would upset my well controlled INR so I only take tiny amounts. No one likes to take medication that rules their choices in life, but I’ve done all right in the three years of having Afib. I tried Dabigatran and ended up in the ER 3 times in 4 months with heartburn so bad I thought I had a perforated ulcer. that’s why I was asking about the effects of CoQ10. Online numerous sites say it interacts. I would like to think the opposite but I’m not willing to risk trying it to see. 🙂

Post ablation, I was put on dabigatran because I couldn’t keep my INR in the zone. That was OK by me because I knew indications are that K supression leads to vascular calcification and weakened bones. I paid for the choice with three weeks of Intestinal Hell, courtesy of this first warfarin alternative. The next alternative, rivaroxaban (read what Dr John says about it), treated me very nicely. No gastrointestinal “issues” – nor any others at all – for the next four months. No K supression consequences. It’s not cheap, but how valuable are the warfarin-effected aspects of your health?

They are to be avoided. I’ll google Dr. J’s thoughts though I’m sure I’ve already read them. Apixaban is available in Canada and that was to be my next try. Thanks.

To Carol McPhee,
“Yogurt is an especially a bad choice for me.”

I mentioned menaquinones, vitamin K2, earlier and I doubt that many (if any) pursued what I said. That includes the doc who originated this commentary opportunity. Literally, the topic of vitamin K2 is sooo novel in this country (but it has been pursued in the Netherlands, Japan and Italy for longer and they are waayy ahead of us in knowledge while we continue to be idiots) that it is basically unknown in our medicine – not to mention that there is no Rx menaquinone here.

‘If pharma don’t got it, NOBODY gots it!’

Go to Mayo or Harvard or our government sites and search menaquinones. You will get either no hits (for the first two) and a weird and incorrect reference(s) from our government. And this nutrient is the one that activates (indirectly) matrix gla protein, the one activated protein that makes for more elastic, youthful arteries and valves! It is the most potent anti-calcification method known, but it is NOT from pharma. It is from nature and Americans known nothing of nature nor how to achieve optimal health. They ‘ask their doctors’ and are led astray. Docs are misinformed because pharma controls the data, FDA is beholden to pharma, and docs are the peddlers of pharma’s crap, even if they really, really mean well. And it is crap.

Yogurt is a fermented food that happens to make vitamin K2. Cheese of the fermented types (Jarlsberg, cheddar, Ementhaler, pecorrino – NOT lousy “American” cheese nor unfermented types like mozzarella though) make various forms of vitamin K2 also. Since you are on the toxin warfarin, you are finding it tough to counter-act it with real foods. You are set up for problems from this. It might take time, but you are calcifying as you read this.

Your warfarin is making for inappropriate calcium deposition, a known side effect. Statins seemingly do this, too, as do bisphosphonates. They ALL block proper vitamin K action in the body. This is a bad thing.

The reason I am bringing up vitamin K is that it is a quinone, just as CoQ10 is a quinone and these are among the EXTREMELY important substances that are biosynthesized in the mevalonate pathway. Statins muck up this pathway because cholesterol is also biosynthesized in this pathway. So statins muck up some of the most powerful and essential substances for heart health, bone health, anti-cancer activities, collagen creation, optimal brain functioning, optimal nervous system functioning, insulin sensitivity maintenance, inflammation suppression, and more.

An interesting couple articles you might enjoy:
Statins use and coronary artery plaque composition: Results from the International Multicenter CONFIRM Resistry (2012)
[Granted, they could have done this better, but this was to be the impetus to see what statins do to plaque…and it doesn’t look good, but needs interventional studies where before statin plaque is evaluated and then after statin administration]
Circulating matrix Gla protein is associated with coronary artery calcification and vitamin K status in healthy women (2012)

Or read the book from a pharma shill, Triumph of the Heart. In it, he admits that pharma considered adding CoQ10 to statins but for some reason did not. They, too, did not know about vitamin K2 at all. Hell, no one seems to.
And admitting how terrible statins are will be very awkward for many. But they are truly terrible. Only middle-aged men who have had a cardiovascular event benefit, yet 75% of these terrible prescriptions are for ‘prevention.’ BS It is all a big, big and very lucrative lie.

or go to PubMed and start rooting around. Look at the triage theory vitamin K, look at warfarin and calcium, learn about menaquinones. Even learn about fermented foods! Two really new articles are admitting what I have said above: more K2 means better health, but they look at fermented foods as probiotics instead of understanding that, indeed, the ‘critters’ of fermented foods DO make it to our gut and affect OUR microbiome and this is a good thing, but they do not seem to know that some fermented foods make vitamin K2, long chain menaquinones, and this is extremely important. Fermented foods are found in all the cultures with the best health and longevity. They are distancing themselves from us in terms of IQ, health costs, and more because they have real food, whereas we do not in the US. We have a food industry along with a medical industry that, in cahoots whether they know it or not, are harming us irreparably.

Learn about nattokinase. It is an alternative that may really help you.

Carol, that’s a hoot! I can identify . . . . . . .

By the way, here in the states, Bayer has a plan to help patients get Xarelto for very low cost for the first year. I believe it’s tied into private insurance plans only, though, so I’m not sure if it’s offered with any type of government run program. You might look into it up there, though.

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