From The July 1999 Issue of Nutrition Science News
By Carmia Borek, Ph.D.
Among the most popular antioxidant nutrients being requested by consumers is Co-Q10, which stands for coenzyme Q10, a fat-soluble cofactor in metabolism that plays a key role in the lives of cells. The better varieties come in an oil-based, solubilized, gelatin-capsule form, which studies show is more bioavailable in humans than powder-based forms of the nutrient. [1,2]
Co-Q10 has a dual function. On one hand, it is essential for generating energy in mitochondria, the energy centers of virtually every cell. On the other hand, it is part of the cell antioxidant defense system, which protects against toxic oxygen by-products made during metabolism.  Co-Q10 is made in human cells and is found in the cells of animals and plants that comprise our daily diet. Because of its widespread and ubiquitous presence, Co-Q10 is also called ubiquinone.
Co-Q10 was isolated from heart mitochondria in 1957 at the University of Wisconsin, Madison, and identified as an electron transporter due to its ability to transport electrons through the mitochondrial membrane.  This occurs in a chain process of respiration in which the energy molecules from foods are burned (oxidized) by the oxygen we breathe to produce the energy units of adenosine triphosphate, or ATP.
Co-Q10 has antioxidant actions similar to those of other fat-soluble antioxidants such as vitamin E, scavenging free radicals and preventing oxidation of lipids and other molecules. In test-tube experiments, Co-Q10 helps maintain the antioxidant state of vitamin E and possibly does so in the body.  Chemoprotective effects of Co-Q10 were reported recently in a small study of 24 production workers in Poland's paint and lacquer industry who had elevated serum concentrations of oxidized lipids. Although few details were given, the study concluded that four weeks of Co-Q10 supplementation helped reduce blood levels of lipid peroxidation products after exposure to the free radical-producing chemicals. 
With age, damage from free radicals accumulates in tissues, increasing susceptibility to many diseases and age-related conditions. Aging is also associated with a decrease in Co-Q10 levels both inside and outside mitochondria, which affects antioxidant protection and energy.  The brain, heart and muscles, richest in mitochondria, are most affected by this age-related decline.
Neuroprotection With Co-Q10
Free radical damage and defects in energy metabolism are linked to the development of various brain diseases, suggesting that supplementation with Co-Q10 may have important therapeutic effects. 
Recent animal studies at Massachusetts General Hospital in Boston show that oral Co-Q10 supplements enter the brain, protect against neurodegenerative diseases, and prolong life in animals with defective mitochondria. 
In one study, researchers gave Co-Q10 at 200 mg/kg body weight daily for two months to both young rats (one to two months) and older rats (12 to 24 months). The average life span of a rat is between 24 and 36 months. In the older rats, supplementation doubled blood levels of Co-Q10 and increased Co-Q10 in the brain by 30 to 40 percent. This change restored the lower Co-Q10 levels of the older rats to levels seen in young animals. Young rats also showed increased Co-Q10 levels in the blood but not in the brain.
These results suggest that whereas the older rat brain can absorb more Co-Q10, the Co-Q10 content of the brain in the younger rats was at its maximum level and could not increase further, even when blood levels were increased. The studies positively show that Co-Q10 supplements can increase the levels in brain mitochondria, where Co-Q10 is especially concentrated.
In other studies, important findings point to the potential therapeutic effects of Co-Q10 supplementation on patients with particular neurodegenerative diseases. One such example is Huntington's disease, a genetic human disease characterized by a loss of nerve cells. Scientists believe that one cause of the illness may be defective energy metabolism and oxidative stress that lead to the slow degeneration of nerve cells. Recent studies of rats with a form of Huntington's disease produced by toxins against mitochondria show that feeding the diseased animals Co-Q10 increased antioxidant levels in brain mitochondria and reversed some of the disease conditions.  These findings strengthen the prospect for Co-Q10 treatment in patients not only with Huntington's disease but also other neurodegenerative diseases such as Parkinson's and Alzheimer's diseases.
Other Massachusetts General Hospital studies showed that daily Co-Q10 supplementation of 200 mg/kg body weight increased the life span of mice who had a genetically induced defect in mitochondria, as compared to controls that had the same defect but did not receive Co-Q10 in the diet.  These results show that supplementation with Co-Q10 preserved mitochondrial function in the genetically damaged mice and prolonged their life.
Studies in normal rats and mice, however, showed that lifelong daily supplementation of Co-Q10 (10 mg/kg body weight) did not prolong or shorten their life span compared with those that did not receive Co-Q10.  The researchers found a 2.6- to 8.4-fold increase in Co-Q10 in the blood and liver but not in the heart, kidney or brain of the animals at all ages. The results differ from the life-prolonging effects of 200 mg Co-Q10 reported above. They suggest the possibility that 10 mg/kg Co-Q10 may be enough to raise blood levels in the rats but too low to enhance levels in the brain and other organs and prolong life.
Vascular and Cardio Effects
Progressive oxidative damage of low-density lipoprotein (LDL) cholesterol forms fatty streaks and plaques in the arteries and leads to atherosclerosis. Plaques can dislodge and form a clot that may block brain arteries and trigger a stroke or block coronary arteries and cause a heart attack. In its antioxidant capacity, Co-Q10 helps protect LDL from oxidation, thereby reducing the risk of the cascading events that may lead to these conditions. 
Stroke and severe neuronal damage can be caused by insufficient blood (ischemia) to the brain and a resulting lack of oxygen (ischemic hypoxia). A study of rats with experimentally induced ischemia showed that 10 mg/kg body weight of Co-Q10 reduced most neuronal damage in the brain. These results indicate the important antioxidant actions of Co-Q10 in protecting the brain against the damaging consequences of ischemia. 
Since the heart is rich in mitochondria, Co-Q10 supplements may give heart mitochondria the boost they need in cases where the heart is failing. A number of clinical trials have shown the benefits of Co-Q10 for patients with heart conditions.
In one study, 73 patients who had suffered a severe heart attack were treated with Co-Q10, 120 mg daily for 28 days, while 71 other acute heart-attack patients served as the placebo group. Treatment with Co-Q10 showed significant cardiac protection in these patients. After treatment, compared to placebo the Co-Q10 group showed a two- to threefold reduction in severe chest pain and in heart arrhythmia and improvement in heart function, as well as a reduction in subsequent heart-attack deaths and in nonfatal heart attacks. In addition, markers of oxidative stress, such as products of lipid peroxidation, were reduced in the Co-Q10 group, and levels of antioxidant vitamins A, C and E increased. The conclusion was that if Co-Q10 is given to a heart patient within three days after the onset of symptoms, rapid cardiac protection is achieved. 
Another study of 424 patients with six forms of heart disease, conducted between 1985 and 1993, showed that supplementing with 75 - 600 mg a day (242 mg average) of Co-Q10 produced a significant improvement in heart function. Before taking Co-Q10, most patients were taking one to five cardiac medications; by the end of the study 43 percent stopped taking between one and three drugs, while only six percent of patients required the addition of one drug. Researchers concluded that Co-Q10 produced "gratifying" clinical responses in treating a broad range of heart diseases while easing the financial and medical burden of other medications. 
Co-Q10 is part of the antioxidant defense force that protects all tissues and plays an important role in reducing the risk of disease and age-related conditions. [1,10]Because studies show oil-based, solubilized forms provide greater bioavailability, recommend these types to your customers.
The ABCs of Co-Q10
1. Chopra RK, et al. Relative bioavailability of coenzyme Q10 formulations in human subjects. Int Vitam Nutr Res 1998;68:109-13.
2. Ozawa Y, et al. Intestinal absorption enhancement of coenzyme Q10 with a lipid microsphere. Arzneimittelforschung 1986 Apr;36(4):689-90.
3. Frei B, et al. Ubiquinol-10 is an effective lipid-soluble antioxidant at physiological concentrations. Proc Natl Acad Sci USA 1990 Jun;87(12):4879-83.
4. Crane PL, et al. Isolation of a quinone from beef heart mitochondria. Biochem Biophys Acta 1957;25:220-2.
5. Kagan VE, et al. Antioxidant effects of ubiquinones in microsomes and mitochondria are mediated by tocopherol recycling. Biochem Biophys Res Communic 1990;169:851-7.
6. Dlugosz A, Sawiska E. The chemoprotective effects of coenzyme Q10 on lipids in the paint and laquer industry. Int J Occup Med Environhealth 1998;11;153-63.
7. Lenaz G, et al. Oxidative stress, antioxidant defenses and aging. Biofactors 1998;8:195-204.
8. Russel T, et al. Coenzyme Q10 administration increases brain mitochondrial concentration and exerts neuroprotective effects. Proc Nat Acad Sci 1998;95:8892-7.
9. Lonnort K, et al. The effects of lifelong ubiquinone Q10 supplementation on the Q9 and Q10 tissue concentrations and life span of male rats. Biochem Mol Biol Int 1998;44:727-37.
10. Neuzil J, et al. Alpha-tocopherol hydroquinone is an efficient multifunctional inhibitor of radical-initiated oxidation of low density lipoprotein lipids. Proc Natl Acad Sci USA 1997;94:7885-90.
11. Ostrowski RP, et al. Evaluation of morphological changes after treatment with coenzyme Q10 in endothelin-1 induced experimental ischemia in the rat. Folia Neuropathol 1998;36:185-8.
12. Singh RB, et al. Randomized double blind placebo-controlled trial of coenzyme Q10 in patients with acute myocardial infarction. Cardiovasc Drugs Ther 1998;12:347-53.
13. Langsjoen H, et al. Usefulness of coenzyme Q10 in clinical cardiology: a long term study. Mol Aspects Med 1994;15 Suppl:s165-75
Carmia Borek, Ph.D., is a research professor at Tufts University School of Medicine in Boston. She is author of Maximize Your Health-Span with Antioxidants: The Baby-Boomer's Guide (Keats Publishing, 1995).