Coenzyme Q10

Overview

Coenzyme Q10, also known as ubiquinone, is found in the mitochondria, and it is essential for energy production. It is classified as an antioxidant, although it has been suggested that it should be classified as a fat-soluble vitamin.

An increasing body of research is demonstrating that supplementation with coenzyme Q10 can be beneficial in the treatment of a number of health problems, particularly cardiac conditions and diseases. Studies have suggested that supplementation may be beneficial in the treatment of breast cancer, diabetes mellitus, immune deficiency, muscular dystrophy, and periodontal disease.

Deficiency primarily affects the heart and may lead to heart failure. Deficiency can result from impaired coenzyme Q10 synthesis or increased needs from diseases such as angina, hypertension, and congestive heart failure. Additionally, coenzyme Q10 levels may decrease as part of the aging process.

Dietary Sources

Coenzyme Q10 is found in every plant and animal cell, hence the alternative name, ubiquinone. Primary dietary sources include oily fish, organ meats, and whole grains.

Constituents/Composition

Coenzyme Q10 is a component of the mitochondria within each cell. It is a coenzyme and an antioxidant involved in the process of creating ATP, and thus critical to providing useable energy to the body.

Commercial Preparations

Coenzyme Q10 is available commercially in many forms including the following.

• Softgel capsules containing coenzyme Q10 suspension in oil (soybean oil); solubilized (Q-Gel) (good bioavailability)
• Powder-filled hardshell capsules
• Powder-based tablets

Therapeutic Uses

• Coenzyme Q10 can reverse or prevent degenerative lesions of the heart associated with angina, hypertension, and congestive heart failure by providing optimal nutrition at the cellular level.
• Congestive heart failure: Coenzyme Q10 as an adjunct to conventional drug therapy has been demonstrated to improve symptoms such as cyanosis, edema, venous congestion, heart palpitations, sweating arrhythmia, vertigo, and insomnia, in patients with moderate to severe CHF. Coenzyme Q10 alone may be sufficient to improve symptoms in patients with mild CHF.
• Hypertension: 39% of patients with hypertension have a coenzyme Q10 deficiency; studies have shown that coenzyme Q10 supplementation lowers HBP after 4 to 12 weeks. Coenzyme Q10 is not a typical antihypertensive drug; it apparently corrects a metabolic abnormality that favorably affects blood pressure.
• Angina: May reduce anginal episodes and improve cardiac function.
• Myocardial infarction: May provide protective effects in patients with acute myocardial infarction if administered within three days of onset of symptoms.
• Arrhythmia: May be beneficial in controlling cardiac arrhythmia.
• Ischemia: Acute intravenous coenzyme Q10 improves function and efficiency and decreases oxidant injury after cardiac ischemia and reperfusion.
• Cardiomyopathy: May be beneficial for cardiomyopathy by increasing cardiac ejection fraction, reducing shortness of breath, and increasing muscle strength.
• Mitral valve prolapse: One study has demonstrated that heart function returns to normal when coenzyme Q10 is taken for at least 8 weeks in doses of 2 mg per kg of body weight. When taken for 18 months or more, relapse rarely occurred; however, when taken for only 12 to 17 months, there were more frequent relapses.
• Cardiac bypass surgery: Pretreatment supplementation with coenzyme Q10 has been shown to reduce oxidative damage and protect the heart during surgery.
• Breast cancer: In Danish studies, coenzyme Q10 in dosages of 390 mg per day, as part of a nutritional protocol, was found to support at least partial remission, tumor reductions, and retarded metastasis.
• Chemotherapy: Coenzyme Q10 reduces the cardiotoxicity of adriamycin.
• Diabetes mellitus: In one study, coenzyme Q10 reduced fasting blood sugar by at least 20% in 14 of 39 patients, and by at least 30% in another 12 of 39 patients; ketone bodies fell by at least 30% in 13 of 22 patients.
• Exercise/weight loss: May be beneficial in improving capacity at submaximal heart rate, maximal work load, maximal oxygen consumption after about four weeks of supplementation. May assist in weight loss by correcting energy consumption and expenditure balance in certain individuals.
• Immune deficiencies: Supplementation with coenzyme Q10 may enhance immune response.
• Mitochondrial and neurodegenerative diseases: Coenzyme Q10 supplementation may improve energy production in muscle cells, thereby improving physical performance.
• Periodontal disease: Coenzyme Q10 deficiency in gingival tissue is present in 60 to 96 percent of patients with periodontal disease. Low levels of coenzyme Q10 may indicate a systemic imbalance, or a response to the periodontitis itself. Oral treatment with coenzyme Q10 reverses the gingival tissue deficiency and appears to accelerate healing by correcting abnormal citrate metabolism and by generally improving energy-dependent healing and repair.

Dosage Ranges and Duration of Administration

General supplementation dose is 25 mg bid.

Experimental doses:

• 100 mg/day in patients with congestive cardiomyopathy
• 60 mg/day for four to eight weeks to enhance athletic performance
• 120 mg/day for 28 days in patients with acute myocardial infarction
• 400 mg per day for potential prevention and treatment of breast cancer, and possibly other forms of cancer

Coenzyme Q10 should be taken with a meal with oil since it is oil soluble. Absorption decreases in the absence of oil.

Side Effects/Toxicology

Coenzyme Q10 appears to be safe with no significant side effects.

Warnings/Contraindications/Precautions

Coenzyme Q10 appears to be safe; however, there have been no studies pertaining to safety during pregnancy and lactation.

Interactions

Daunorubicin; Doxorubicin

CoQ10 protected against cardiac toxicity associated with anthracyline treatment in patients with malignancy. In one study, children with acute lymphoblastic leukemia or non-Hodgkin's lymphoma who received CoQ10 (100 mg po bid) with daunorubicin exhibited significantly fewer signs of cardiac dysfunction compared to treatment with daunorubucin alone (Iarussi et al. 1994). Mice treated with a combination of doxorubicin and CoQ10 survived significantly longer (224.1%) than controls; the optimum protective effect was achieved with oral doses of 10 mg/kg/day (Shinozawa et al. 1996). The CoQ10 group had significantly less liver and heart microsomal lipid peroxidation, a potential indicator of cardiac toxicity.

Diltiazem; Enalapril; Isosorbide Dinitrate; Isosorbide Mononitrate; Metoprolol; Nitrendipine; Nitroglycerin

In a randomized, double blind trial, patients with coronary artery disease (CAD) were treated with conventional antihypertensive medications and either CoQ10 (60 mg bid) or B vitamin complex for 8 weeks (Singh et al. 1999). Patients treated with CoQ10 required lower doses of their antihypertensive medications (diltiazem, metoprolol, enalapril maleate, and nitrate). In spontaneously hypertensive rats, chronic pretreatment with CoQ10 (10 mg/kg) prolonged, but did not enhance, the antihypertensive effects of enalapril and nitrendipine (Danysz et al. 1994). More research is needed to determine if CoQ10 affects individual medications.

Pentoxifylline

The combination of pentoxifylline and CoQ10 (10 mg/kg) in rats was more effective than pentoxifylline alone at preventing the decrease in hepatic glutathione levels along with the elevation in lipid peroxidation that is typically associated with ischemia-reperfusion damage in the liver (Portakal and Inal-Erden 1999).

Timolol

In one study, ten patients with glaucoma were concomitantly administered CoQ10 (90 mg/day po) with either timolol or saline for six weeks (Takahashi et al. 1989). CoQ10 reduced cardiovascular side effects by diminishing the beta-blocking action of timolol without affecting intraocular pressure.

Warfarin

Case reports have suggested that CoQ10 decreases the anticoagulant effect of warfarin (Landbo and Almdal 1998; Spigset 1994). In one report, three patients had decreased international normalized ratios (INR) after CoQ10 was added to their warfarin regimens (Spigset 1994). The INR of two of the patients dropped after two weeks of CoQ10 supplementation (30 mg/day). Oral administration of CoQ10 (10 mg/kg/day) for 8 days substantially decreased serum concentrations of warfarin (1.5 mg/kg) and significantly increased levels of major metabolites in rats (Zhou and Chan 1998). CoQ10 may increase the hepatic metabolism of warfarin and thereby reduce its anticoagulant effect.

References

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