Robin Koon

February 26, 2013

7 Min Read
CoQ10 Supplementation with Statins

Hypercholesterolemia (high cholesterol levels) is associated with an increased risk of coronary heart disease, myocardial infarction, peripheral vascular disease and stroke. Although the death rates from cardiovascular disease (CVD) have declined, the burden of disease remains high. More than 2.200 Americans die of CVD each day (one death every 39 seconds); 785,000 Americans will have a new coronary attack and 795,000 Americans will have a new or recurrent stroke each year.

One of the reasons cardiac deaths have lowered since the 1990s is the reduction of cholesterol levels. To lower cholesterol levels, physicians are prescribing statin drugs. An estimated 36 million Americans are now using statin drug therapy. It is well documented that statin drugs can lower serum coenzyme Q10 (CoQ10) levels.


Statin drugs (HMG-CoA reductase inhibitors) are a class of prescribed drugs used to lower cholesterol (hypercholesterolemia). These drugs are one of the most effective ways to lower low-density lipoprotein (LDL) cholesterol plasma levels. Lowering cholesterol has been shown to have a significant benefit on cardiovascular morbidity and mortality, especially in patients with or at-risk for coronary heart disease (CHD). Statins have become the second largest prescribed drugs class in the United States.

Statins lower cholesterol by inhibiting the liver enzyme HMG-CoA reductase in the melvonate pathway. The mevalonate pathway is a metabolic pathway that produces cholesterol, sterols and other isoprenoids. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, an early and rate-limiting step in cholesterol biosynthesis.

The endpoints of the melvonate pathway include cholesterol (bile salts, steroid hormones and hedgehog proteins), ubiquinone (coenzyme Q10), dolichol, heme A, vitamin D, squalene, and farnesyl and geranylgeranyl proteins. All of these compounds are reduced when taking statin drugs.

Although statins are generally well-tolerated, adverse effects may occur in some patients. The most common problems include diarrhea, abdominal pain, stomach cramps, dizzy spells, slight fever, headaches, etc. These are usually mild and go away in a matter of hours. The most common adverse side effects are elevated liver enzymes or myalgia (muscle pain, cramps, weakness, or fatigue) after taking a dose (5 to 10 percent), and are dose dependent. Elevated creatine kinase (CK), hepatic transaminases, insomnia, erectile dysfunction and allergic reactions are possible but rare. Myopathy (proximal muscle weakness/tenderness), myositis (muscle weakness with elevated CK levels), and rhabdomyolysis (a serious complication) are potential side effects, but the only occur in 0.1 to 0.2 percent of users. Statins may adversely affect cognition in patients with dementia. Tendinitis and tendon rupture in association with statin use have also been documented.

Drug therapy for hypercholesterolemia has remained controversial mainly because of insufficient clinical trial evidence for improved survival. Although there is a large body of evidence that links elevated blood cholesterol levels to CHD, concerns remain about the strength of the evidence for a cause-and-effect relationship. Questions still remain regarding the exact relationship between blood cholesterol and heart disease.


The most common coenzyme in human mitochondria is CoQ10. The compound is a fat-soluble vitamin-like essential nutrient that is naturally present in every cell of the body. Its primary responsibility is for the production of cellular energy (ATP), the source of the bodys energy. CoQ10 is an essential cofactor in mitochondrial oxidative phosphorylation, and is necessary for ATP production. The electron and proton transfer functions of CoQ10 are fundamentally important to all life forms.

Approximately half of the bodys CoQ10 is obtained through dietary fat ingestion, with the remainder coming from endogenous synthesis. Practically every cell has the ability to synthesize CoQ10, but it is mostly synthesized in the liver. The endogenous biosynthesis of CoQ10 is a complex process requiring numerous nutrients; the process has 17 steps, requiring at least seven vitamins (vitamin B2 (riboflavin), vitamin B3 (niacinamide), vitamin B6, folic acid, vitamin B12, vitamin C and pantothenic acid) and several trace elements. The CoQ10 molecule has two parts: the benzoquinone ring and the isoprenyl side chains (terpinoid "tail"). The benzoquinone (quinone ring structure) is derived from the amino acids, tyrosine or phenylalanine. The isoprenoid side chain is synthesized from acetyl-CoA through the mevalonate pathway.

Statins and CoQ10

One of the primary side effects of statin drugs is myalgia, which often causes patients to decrease the dosage of the statin or discontinue it. Different mechanisms have been proposed to explain the reason for statin-induced myopathy (e.g., dose related, drug interactions, a reduction of mevalonate pathway products, induction of apoptosis, mitochondrial dysfunction, genetic predisposition, etc.). One of the endpoints of the melvonate pathway products is ubiquinone (CoQ10). One of the prevailing theories is that statin therapy reduces CoQ10 levels in muscle mitochondria (approximately 20 to 35 percent), which leads to myalgia. Since statins reduce cholesterol, we know they also reduce the endogenous production of CoQ10, since both share the same metabolic pathway.

Some researchers think taking a CoQ10 supplement may reduce the risk of these side effects. CoQ10 serum levels are depleted during statin therapy, mainly when statins are taken at higher doses and most markedly with a pre-existing CoQ10 deficiency (such as in the elderly and in heart failure patients). A deficiency in CoQ10 can cause issues with heart health, metabolism and energy production.

Supplementation can raise the circulating serum levels of CoQ10, but the current observational and limited randomized data on the effect of CoQ10 supplementation on myopathic or myalgia symptoms are few, contradictory (mixed results) and inconclusive. Several small clinical trials have suggested CoQ10 in doses of 100 to 200 mg/day may help prevent statin-related muscle side effects. Since no large studies have confirmed this theory, the current U.S. medical guidelines don't recommend routine use of CoQ10 in people taking statins.

No Warning

No official warnings appear in the United States regarding CoQ10 depletion from taking statin drugs, despite several physicians requesting it. Other countries do provide a warning. For example, labeling in Canada clearly warns of CoQ10 depletion and even points it out in several statin drug inserts (e.g., Canadian: Mevacor®, Pravachol® & Lipitor®), which state:

"Effect on Ubiquinone (CoQ10) Levels -  ignificant decreases in circulating ubiquinone levels in patients treated with statins have been observed. The clinical significance of a potential long-term statin induced deficiency of ubiquinone has not been established. It has been reported that a decrease in myocardial ubiquinone levels could lead to impaired cardiac function in patients with borderline congestive heart failure."

CoQ10 is an essential nutritional factor, not a drug, hindering its acceptance by most clinicians. When the drug company Merck released the first statin drug (Mevacor®) into the marketplace (FDA approved it in 1987), they were aware of the CoQ10 deficiency its use causes. They even filed two patents for combinations of statins and CoQ10. These two patents (no. 4,933,165 and no. 4,929,437) held by Merck expired in May and June 2007.

Currently, evidence is insufficient to prove the etiologic role of CoQ10 deficiency in statin-associated myopathy. Large, well-designed clinical trials are needed to address this issue. However, it is a logical deduction is to consider complementing statin therapy with CoQ10 to support a potential significant deficiency.

The following is a list of statin drugs currently in the U.S. marketplace:

  • Advicor® (niacin extended-release/lovastatin)

  • Altoprev® (lovastatin extended-release)

  • Caduet® (amlodipine and atorvastatin)

  • Crestor® (rosuvastatin)

  • Juvisync® (sitagliptin/simvastatin)

  • Lescol® (fluvastatin)

  • Lescol XL (fluvastatin extended-release)

  • Lipitor® (atorvastatin)

  • Livalo® (pitavastatin)

  • Mevacor® (lovastatin)

  • Pravachol® (pravastatin)

  • Simcor® (niacin extended-release/simvastatin)

  • Vytorin® (ezetimibe/simvastatin)

  • Zocor® (simvastatin)

 Learn more about Co10 and find suppliers in INSIDER's CoQ10 Buyers Guidebook.

Robin Koon, executive vice-president at Best Formulations, has more than 25 years of pharmaceutical experience in clinical pharmacy as a retail drug chain executive overseeing operations and in managed-care.

About the Author(s)

Robin Koon

Robin Koon is executive vice president at Best Formulations , and has more than 35 years of pharmaceutical experience in clinical pharmacy, as a retail drug chain executive, in managed-care and in manufacturing.


Subscribe and receive the latest insights on the health and nutrition industry.
Join 37,000+ members. Yes, it's completely free.

You May Also Like