Coenzyme Q10 is a compound found in all human cell membranes and mitochondria. Mitochondria are tiny organs suspended in the cytosol (the semifluid portion) of cells and are considered the cells' powerhouses because they produce adenosine triphosphate, a molecule that stores and transports energy within the cell. Coenzyme Q10, also known as ubiquinone or Co-Q10, helps fuel the body by regulating the chemical reactions within the mitochondria1,2 that convert food into usable energy3. It also helps mitochondria create energy,3 and its reduced form, ubiquinol, serves as an antioxidant by protecting cell membranes from peroxidation, a process where free radicals "steal" electrons, resulting in cell damage.4,5,6
Co-Q10, which is synthesized within the body's cells, can also be obtained through diet.7 Decreased levels of Co-Q10 in serum, or tissue, can result from an insufficient dietary intake (from anorexia, cachexia or chronic malnutrition), impairment in Co-Q10 biosynthesis, excessive utilization of Co-Q10 by the body,8 gene mutation, aging, cancer drugs and statins (drugs used to treat high cholesterol). People with low Co-Q10 levels may need a daily supplement of 100 mg of the nutrient.9,10
Co-Q10 deficiency in adults can cause adult-onset cerebellar ataxia (a disorder of the nervous system that affects balance and coordination) or myopathy (a neuromuscular disease that creates weak muscles).7 In infants and children, Co-Q10 deficiency, which is caused by a rare yet treatable mitochondrial disorder, may cause cerebellar ataxia, myopathy, epilepsy, mental retardation, cardiomyopathy (heart muscle disease) and nephropathy (a kidney disorder).11
Researchers have also examined Co-Q10 supplementation in patients with congestive heart disease,17,18 Parkinson's disease19,20,21,22 and type 2 diabetes,23,24,25 but further research is needed before making definitive conclusions about using Co-Q10 for these patients.
Hypertension is prevalent in the U.S., and many people seek alternatives to commonly prescribed medications. Because of its performance in clinical trials, Co-Q10 is one potential alternative.
In a 12-week randomized, double-blind, placebo-controlled study, hypertensive subjects (46 men, 37 women) were given either 60 mg of Co-Q10 twice a day or a placebo. The Co-Q10 group experienced an average reduction in systolic blood pressure of 17.8 mm Hg, ?7.3 mm Hg.12
A meta-analysis of 12 clinical trials (362 total patients) that examined the use of Co-Q10 for hypertension assessed overall effectiveness, consistency of treatment and side effects from supplementation. Three randomized controlled trials (100 to 120 mg of Co-Q10 a day in 120 subjects), one crossover study (100 mg a day of Co-Q10 in 18 subjects) and eight open-label studies (doses ranged from 30 to 225 mg per day of Co-Q10 in 214 subjects) were included in the analysis. The authors concluded that Co-Q10 may potentially lower systolic blood pressure by up to 17 mm Hg and diastolic blood pressure by up to 10 mm Hg without significant side effects in hypertensive patients.13
In a randomized study, 74 people with type 2 diabetes and dyslipidemia (elevated "bad" cholesterol) were given either 100 mg of Co-Q10 twice a day, 200 mg of fenofibrate (a cholesterol-lowering medication) once a day, both or neither, for 12 weeks. Co-Q10 significantly decreased systolic (-6.1 mm Hg ?2.6 mm) and diastolic (-2.9 mm Hg ?1.4 mm) blood pressure, whereas fenofibrate and placebo had no effect on blood pressure.23
Because of Co-Q10's unobjectionable safety profile, it may be a treatment for individuals with mild hypertension.
How safe is Co-Q10 for human use? The supplement's safety was examined in a double-blind, randomized, placebo-controlled study. Eighty-eight healthy adults took Co-Q10 (Kaneka Q10) for four weeks at doses of 300, 600 and 900 mg per day. No serious adverse events were observed in any group, but adverse events were reported by 16 adults taking a placebo, 12 adults on the 300 mg dose, 20 adults on the 600 mg dose and 16 adults on the 900 mg dose. Adverse events reported included common cold symptoms and gastrointestinal distress (abdominal pain and soft feces). This study indicates that there are few serious adverse events related to Co-Q10 consumption at doses ranging from 300 to 900 mg per day.26
Another study also found Co-Q10 to be safe in healthy adults. In a single-blind, placebo-controlled design, healthy subjects were given a single dose of 150 or 300 mg of Co-Q10. Later, they were supplemented with either 90, 150 or 300 mg of Co-Q10 daily for four weeks. In both instances, standard laboratory tests, vital signs, electrocardiogram and physical examination showed no clinically relevant changes, indicative of no negative side effects.27
Co-Q10 as an antioxidant
In its reduced form as ubiquinol, Co-Q10 functions as an antioxidant by regenerating active forms of ascorbic acid and alpha-tocopherol (vitamins C and E, respectively) in the body, by regulating cell membrane fluidity and by protecting phospholipids (the structural components of cell membranes) against peroxidation.14
Oxidized low-density lipoprotein particles have been strongly associated with coronary artery disease.28 Both alpha-tocopherol and ubiquinol play essential roles in preventing LDL particle oxidation. Alpha-tocopherol is the most prevalent antioxidant found in LDL particles, with concentrations 20 to 300 times greater than other antioxidants. In-vitro tests indicate that the oxidation resistance of LDL increases linearly with the quantity of vitamin E in LDL particles.29 Studies in mice show that Co-Q10 decreases the concentration of lipid hydroperoxides (rancid fat molecules) in atherosclerotic lesions while also minimizing the size of atherosclerotic lesions in the aorta.15 Atherosclerotic lesions are weaknesses in artery walls caused by the walls' loss of elasticity.
Co-Q10 shows promise as an anti-atherosclerotic supplement; however, larger clinical trials in humans should be conducted to assess its potential for reducing LDL oxidation and size of atherosclerotic lesions.
Statin drugs are among the most effective medications available for reducing LDL cholesterol.30 However, adverse effects from statin use may include myositis (inflammation of the muscles), myopathy and, rarely, rhabdomyolysis (breakdown of skeletal muscle).31
Statin drugs interfere with the production of Co-Q10 and, because of Co-Q10's role in mitochondrial energy production, statin-related Co-Q10 deficiency may play a role in myopathy.30
While reviewing studies examining statin treatment and Co-Q10 levels, researchers found nine observational studies and six randomized, controlled trials that demonstrate that statin therapy reduces plasma/serum Co-Q10 levels by 16 percent to 54 percent. These decreases may be related to decreases in LDL because LDL is one of the compounds that transports Co-Q10 in the body.30
The largest and longest clinical trial yet to examine the relationship between statins and Co-Q10 used a double-blind, placebo-controlled design. In this trial, 1,049 patients with high blood cholesterol, aged 18 to 80 years, were randomized to receive either 10 mg a day of atorvastatin (the component in the drug Lipitor), 20 mg a day of lovastatin (Mevacor, Altacor), or a placebo, for one year. Sixteen weeks into the trial, the participants receiving a placebo were randomly placed into either the atorvastatin or lovastatin group. At 52 weeks, the atorvastatin group had a 37 percent reduction in LDL cholesterol, and the lovastatin group had a 29 percent reduction. Total cholesterol decreased 27 percent and 21 percent for the atorvastatin and lovastatin groups, respectively. Ubiquinone (Co-Q10) levels decreased in a similar manner to decreases in LDL, with the decrease in ubiquinone greater in the atorvastatin versus lovastatin treatment groups (38 percent and 27 percent, respectively).32
In another clinical trial that also examined changes in intramuscular Co-Q10 levels, 49 patients with high blood cholesterol were randomized to receive 80 mg a day of simvastatin (the component in the drug Zocor), 40 mg a day of atorvastatin or a placebo, for eight weeks. At the end of the eight-week period, the simvastatin group's intramuscular (not blood plasma) cholesterol concentrations increased nonsignificantly, and their muscle ubiquinone concentration decreased significantly; no change was noted in both the atorvastatin and placebo groups.33
In another study, simvastatin was shown to have no effect on muscle Co-Q10 levels. In this six-month trial, 19 patients with high blood cholesterol were given 20 mg a day of simvastatin. Muscle biopsies showed no significant changes in ubiquinone concentrations from baseline to post-test.34
Collectively, these studies indicate that the decrease in Co-Q10 that results from statin use corresponds to the decrease in LDL and total cholesterol; the concentration of Co-Q10 to LDL and total cholesterol remains roughly the same. In addition, low-dose statins do not seem to decrease intramuscular Co-Q10 levels. There is little human data, however, examining the relationship between statin-induced myopathy and Co-Q10. Studies on animals indicate that statin-associated myopathy, and subsequent muscle injury, can occur independently of decreases in intramuscular Co-Q10.30 (See table for a summary of which statins at what durations and dosages create Co-Q10 deficiencies.)
Can Co-Q10 supplementation im?prove symptoms of myopathy? In a randomized, double-blind study, 32 patients with statin-related myopathic symptoms were given either Co-Q10 (100 mg per day) or vitamin E (400 IU per day) for 30 days. Muscle pain decreased significantly (40 percent) and pain interference with daily activities also decreased significantly (38 percent) in the Co-Q10 group. There were no significant differences from baseline to post-test in pain or pain severity in the placebo group. This study supports the potential for Co-Q10 as a treatment option for those with statin-related myopathy.16
Co-Q10 may reduce blood pressure in people with mild hypertension. Because of its safety profile, it may be a promising supplement for people with mild risk factors for cardiovascular disease. Co-Q10 functions as an antioxidant, and therefore may reduce LDL oxidation and the size of atherosclerotic lesions. However, more clinical trials in humans should be conducted before people self-prescribe Co-Q10 to alleviate atherosclerosis. Although plasma and serum Co-Q10 levels decrease in patients taking statins, it's unclear if this decrease is related to statin- induced myopathy; therefore, the data do not support routinely recommending Co-Q10 supplementation for patients taking statins.
Marie Spano, R.D., is vice president of the International Society of Sports Nutrition, a freelance writer and a food and supplements consultant.
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