What is CoQ10?Heart Energy Engine and More......
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 What is CoQ10? Chemical Structure of Coenzyme Q10.
Introduction: Coenzyme Q10.
Benefits of Coenzyme Q10 or CoQ10(Co Q 10).
Actions and Pharmacology for CoQ10(Co Q 10).
Coenzyme Q10 in food:
Coenzyme Q10 Deficiency:
Effects of Statin Drugs on CoQ10(Co Q 10):
Supplementation and Safety:
Commercial Production of CoQ10(Co Q 10) Supplements:
Biochemistry of CoQ10(Co Q 10)
Indications and Usage:
Research Update and Findings of Coenzyme Q10
What is CoQ10? Chemical Structure of Coenzyme Q10
Product name : Coenzyme Q10
Synonyms: CoenzymeQ, Co-enzyme Q10, Coenzyme Q (50), CoQ, CoQ10, CoQ(50), Co-Q10, CoQ-10, 2,3 dimethoxy-5 methyl-6-decaprenyl benzoquinone,idebenone (synthetic analogue), mitoquinone, Ubiquinone-10, CoQ10, Ubiquinone 50, Ubidecarenone,Neuquinone, Q10, Taidecanone, ubidecarenone, ubiquinone, ubiquinone-10, ubiquinone-Q10, Udekinon, vitamin q10, vitamin Q10.
CAS RN: 303-98-0
Moleclar formula : C59H90O4
Molucular weight : 863.34
Coenzyme Q10 is a fat-soluble nutrient also known as CoQ10, vitamin Q10, ubidecarenone, or ubiquinone. It is a natural product of the human body that is primarily found in the mitochondria, which are the cellular organelles that produce energy. It occurs in most tissues of the human body; however, the highest concentrations are found in the heart, liver, kidneys, and pancreas. Ubiquinone takes its name from a combination of the word ubiquitous, meaning something that is found everywhere, and quinone 10. Quinones are substances found in all plants and animals. The variety found in humans has a 10-unit side chain in its molecular structure. Apart from the important process that provides energy, CoQ10 also stabilizes cell membranes and acts as an antioxidant. In this capacity, it destroys free radicals, which are unstable molecules that can damage normal cells.
Because it is a vitamin-like substance located in virtually every cell, CoQ10 is also known as ubiquinone,from "ubiquitous" to signify its widespread distribution in the human body, and "quinone," a chemical structure with a unique ability to be oxidized and reduced. Found in most living organisms, it is essential to the production of cellular energy and can be both synthesized in the body and derived from dietary sources. There are dietary sources of CoQ10, including meat, poultry and fish, but these sources contain a small amount of CoQ10. Daily intakes from food typically range between 3 to 5 mg/day, which cannot significantly raise blood and tissue levels.
Healthy humans who consume a well-balanced diet have the ability to synthesize coenzyme Q10. Unhealthy individuals and those on an inadequate diet may not synthesize CoQ10 in sufficient quantities. Thus, the biosynthesis of coenzyme Q10 in the human body requires a good diet,one that is high in vitamins, minerals, and other nutrient factors. The NHANES studies reveal that many Americans do not have an adequate diet. Rather, their intake of most water-soluble vitamins (B-complex vitamins and vitamin C), vitamin A and some minerals and trace elements is insufficient. As noted earlier, many of these nutrients are essential for the biosynthesis of coenzyme Q10. In addition, it has been shown that in disease states, nutrients from food sources may not necessarily be absorbed or available. According to some experts, coenzyme Q10 should be considered an essential nutrient, as it is well established that coenzyme Q10 is essential for the health of every cell in the human body.
Coenzyme Q10 resembles vitamin K in its chemical structure. Biochemically, reduced CoQ10 functions much like vitamin E in that it acts as an antioxidant by donating a hydrogen to free radicals. Like vitamins E and K, CoQ10 is also a lipophilic (fat-soluble) molecule. To better explain, it can only be absorbed in the presence of fat, because it is water insoluble. For better CoQ10 absorption, it either has to be introduced in a fat soluble medium or taken with fat in the diet. Many question why CoQ10 should be supplemented, especially since we produce it naturally in the body and obtain it in our food supply. It has been suggested by some clinical data that the body's natural ability to synthesize CoQ10 may diminish as we age. In addition, those with heart disease seem to produce even less, and they are the ones that need it the most.
COQ10, an abbreviation for Coenzyme Q10, is a compound produced naturally by the body. In fact, it is a substance that exists in all life forms, and even certain foods. As its name implies, it assists the functioning of enzymes. Enzymes are proteins that are responsible for speeding up the rate of chemical reactions that take place in our bodies. Vital functions such as our metabolism are dependent upon these chemical reactions, and, therefore, enzymes and coenzymes, such as COQ10.
Coenzyme Q can exist in three oxidation states: the fully reduced ubiquinol form (CoQH2), the radical semiquinone intermediate (CoQH), and the fully oxidized ubiquinone form (CoQ).
Appearance: Yellow to orange crystalline powder
Identification: IR complies (USP28 <197K>)
Dissolve about 50mg of Ubidecarenone in 1mLof ethyl ether, and add 10mL of dehydrated alcohol. To 2mL of this solution, add 3mL of dehydrated alcohol and 2mL of dimethyl malonate, add 1mL of potassium hydroxide solution ( 1in 5) dropwise, and mix: a blue color appears. (USP28)
Water : <= 0.2% (USP28<921> Method I)
Residue on ignition : <= 0.1% (USP28<281>)
Heavy metals : <= 0.002% (USP28 <231> Method II)
Assay : 98.0-101.0% (USP28)
Chromatogrphic purity : Test 1: Sum of all Impurities: <=1.0% (USP28)
Test 2: Sum of all Impurities: <= 1.0% (USP28)
Test 1 and Test 2: Sum of all Impurities: <= 1.5% (USP28)
Introduction: Coenzyme Q10.
Coenzyme Q10 or CoQ10(Co Q 10) is an organic molecule that is naturally synthesized in the liver. According to Dr. Karl Folkers and other experts, humans can biosynthesize coenzyme Q10 from tyrosine through a cascade of aromatic precursors which indispensably require certain vitamins: vitamins B2, B6, B12, folic acid, niacin, and pantothenic acid. CoQ10 is comprised of a quinone ring and a hydrocarbon side chain made up of 10 isoprene units. This side chain is synthesized from acetyl-CoA. The quinone ring is synthesized from the amino acids (tyrosine or phenylalanine) and is responsible for CoQ10 having such powerful antioxidant activity. The reduced form of CoQ10 is able to scavenge free radicals that may cause damage to the body's DNA, proteins, and lipids, opening the door to a host of various diseases including cardiovascular disease, and neurodegerative diseases such as Alzheimer's or Parkinson's.
In these days of screaming headlines, it's important to be cautious of anything that makes claims that seem a bit too good to believe. And yet, in taking time to check the claims for Coenzyme Q10, you will find decades of research and medical studies from several countries around the world. First discovered in 1957, Coenzyme Q10, or simply CoQ10, is also called ubiquinone, a name that signifies its ubiquitous (widespread) distribution in the human body. As a coenzyme, this nutrient aids mitochondria, the powerhouses of cells, in the complex process of transforming food into ATP, the energy on which the body runs. Coenzyme Q10 is a nutrient which has been found to be beneficial for a surprising variety of health problems:
Researchers have explored the effects of coenzyme Q10 supplementation in people with periodontal disease, which has been linked to coenzyme Q10 deficiency. Double-blind studies show that people with gum disease given coenzyme Q10 achieve better results than those given a placebo.
Virtually every cell in the human body contains coenzyme Q10. The mitochondria, the area of cells where energy is produced, contain the most coenzyme Q10. The heart and the liver, because they contain the most mitochondria per cell, contain the greatest amount of coenzyme Q10. Coenzyme Q10 has helped some people with congestive heart failure - an effect reported in an analysis of 8 controlled trials and found in some, although not all double-blind studies. Coenzyme Q10 may take several months to show beneficial effects. People with congestive heart failure who are taking coenzyme Q10 should not stop taking it suddenly, because sudden withdrawal may temporarily aggravate the symptoms of congestive heart failure.
Coenzyme Q10 or CoQ10(Co Q 10) belongs to a family of substances called ubiquinones. Ubiquinones, also known as coenzymes Q and mitoquinones, are lipophilic, water-insoluble substances involved in electron transport and energy production in mitochondria. The basic structure of ubiquinones consists of a benzoquinone "head" and a terpinoid "tail." The "head" structure participates in the redox activity of the electron transport chain. The major difference among the various coenzymes Q is in the number of isoprenoid units (5-carbon structures) in the "tail." Coenzymes Q contain one to 12 isoprenoid units in the "tail"; 10 isoprenoid units are common in animals.
Coenzymes Q occur in the majority of aerobic organisms, from bacteria to plants and animals. Two numbering systems exist for designation of the number of isoprenoid units in the terpinoid "tail": coenzyme Qn and coenzyme Q(x). N refers to the number of isoprenoid side chains, and x refers to the number of carbons in the terpinoid "tail" and can be any multiple of five. Thus, coenzyme Q10 refers to a coenzyme Q having 10 isoprenoid units in the "tail." Since each isoprenoid unit has five carbons, coenzyme Q10 can also be designated coenzyme Q. The structures of coenzymes Q are analogous to those of vitamin K2.
Coenzyme Q10 is also known as Coenzyme Q(5O), CoQ10, CoQ(50), ubiquinone (50), ubiquinol- 10 and ubidecarerone. Chemically, CoQ10 is known as 2, 3-dimethyoxy-5-methyl-6-decaprenyl-1,4-benzoquinone, and its structural formula is:
It is a solid wax-like substance. CoQ10 is the predominant form in humans, and CoQ9 is the predominant form in rats.
Supplemental CoQ10(Co Q 10) is typically derived from tobacco leaf extracts and fermented sugar cane and beets.
Benefits of Coenzyme Q10 or CoQ10(Co Q 10):
 ATP Booster:
The most important role CoQ10 plays in the body is to support the production and function of adenosine triphosphate, or ATP, the metabolic energy on which the body runs. CoQ10 is found primarily within the membrane of a cell organelle called the mitochondrion, which is often referred to as the "power house" of the cell. Mitochondria are affectionately known as this because of their ability to drive the production of ATP. CoQ10 is an important rate-limiting nutrient that is a cofactor in the mitochondrial electron transport chain¡ªthe biochemical pathway in cellular respiration from which ATP is derived. It serves as an electron transport carrier during the processes of respiration and oxidative phosphorylation. Since nearly all cellular activities are dependent upon energy, coenzyme Q10 is essential for the health of all human tissues and organs.
The heart is one of the most metabolically active tissues in the body, thus it requires large amounts of uninterrupted energy. Heart muscle cells have the greatest concentration of mitochondria, and subsequently, more CoQ10 than any other type of cell. Each heart cell can have thousands of mitochondria (5,000 per cell) to meet these energy demands.
COQ10 is needed by every cell in the body to produce energy. This energy is used in countless crucial ways, such as breaking down and digesting our food, healing wounds, and maintaining healthy muscles. Because Coenzyme Q10 is central to the production of energy, it's not surprising that it is found in especially high concentrations in the heart muscle, which requires a tremendous amount of energy to perform its incessant functions.
Coenzyme Q10 or Co Q10 works together with our body's enzymes, especially those in cells that demand large amounts of energy such as heart cells.This popular supplement has many health benefits for the heart: it helps keep the heart muscle strong so it can beat properly more than 100,000 times a day for decades!
Cardiovascular system engine:
Numerous studies indicate coenzyme Q10 also plays an important role in the maintenance of the entire cardiovascular system. As previously mentioned, CoQ10, in its reduced form, plays an important role as an antioxidant nutrient. The antioxidant potential of CoQ10 helps our bodies prevent or delay cellular deterioration. It is this deterioration that is one of the predominant causes of heart disease. CoQ10 is essential for healthy heart function, as well as to protect the veins and arteries from free radical damage. Research has shown that CoQ10 supplementation exerts a sparing effect on vitamin E in healthy subjects. It also reduces levels of lipid peroxidation, the pivotal step in the cause of atherosclerosis, thereby decreasing the risk of cardiovascular diseases.
Much has been attributed to COQ10's ability to strengthen the heart muscle, and prevent heart attacks and heart disease. Indeed, unlike some other nutritional supplements, which have scant scientific evidence of efficacy, Coenzyme Q10 has been proven in multiple major studies to significantly improve the health of patients with congestive heart failure.
Coenzyme Q10 can also help treat heart disease. In a 12-month placebo-controlled study of more than 2,500 patients suffering from heart disease, those who took coenzyme Q10 were shown to have improved symptoms as compared to those who took only placebo.
Studies have also suggested that taking coenzyme Q10 can help those suffering from high blood pressure by lowering the elevated pressure and preventing complications of this condition.
In addition, other studies have revealed that people suffering from cardiovascular disease tend to have low levels of this crucial nutrient, strongly suggesting a link.
Antioxidant and oxidative stress inhibitor:
In addition to its heart-friendly benefits, coenzyme Q10 is also a powerful antioxidant that can neutralize harmful free-radicals. There are studies that suggest that coenzyme Q10 can boost the immune system and help prevent and treat certain forms of cancers.
Several clinical trials have provided evidence supporting the use of supplementation with CoQ10 in the prevention and treatment of various disorders related to oxidative stress. It has been shown that CoQ10's antioxidant properties and its central role in mitochondrial oxidative phosphorylation make it useful as adjunct therapy for cardiovascular diseases such as congestive heart failure (a disease in which the heart does not adequately maintain circulation), hypertension (high blood pressure), cardiomyopathy (heart muscle disease), angina pectoris (chest pain), drug-induced cardiotoxicity, and ventricular arrhythmia. A significant deficiency of CoQ10 was detected in patients with hypertension. A pilot study showed that CoQ10 supplementation at dosages that ranged from 30 to 360 mg/day to patients with hypertension led to an increase in CoQ10 levels and statistically significant decreases in systolic and diastolic blood pressure.
CoQ10 is also gaining notoriety as a helpful dietary supplement for non-cardiac conditions including diabetes, Parkinson's disease, periodontal disease, compromised immune systems, cancer, muscular dystrophy, and chronic obstructive pulmonary disease (COPD). There is substantial evidence that oxidative damage may play a key role in the pathogenesis of neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases. In a recent study, the percent content of the oxidized form of CoQ10 (a marker of oxidative stress) in total CoQ10 (both oxidized and reduced forms) was found to be slightly elevated in Parkinson's disease patients, when compared with normal subjects, suggesting elevated oxidative stress in Parkinson's disease patients.
CoQ10 supports a broad range of functions in the body leading many experts to suggest that CoQ10 should be an integral part of any dietary supplementation program.
Coenzyme Q10 also acts as a nutrient with powerful antioxidant properties. Antioxidants neutralize free radicals, which are highly reactive chemical substances that can damage cellular material, leading to premature aging and disease. Because of the protection it affords, some experts believe it may have a role in treating or preventing certain types of cancers. Indeed, some studies, although not major in scope, have shown this nutrient can help survival rates in those with prostate and breast cancer.
Coenzyme Q10 for a healthy heart:
Ubiquinone, or coenzyme Q10, is an important nutrient. 2 of its primary uses are for those who are taking high cholesterol pills (the statin drugs in particular). Certain lipid-lowering drugs, such as the 'statins' - lovastatin, simvastatin, pravastatin - and gemfibrozil as well as oral agents which lower blood sugar, such as tolazamide and glyburide, cause a decrease in serum levels of coenzyme Q10 and reduce the effects of coenzyme Q10 supplementation. These drugs inhibit the production of coenzyme Q10 by the liver and will cause serious complications unless one supplements coenzyme Q10 back into the diet. A prescription for lipid-lowering statin drugs should always be accompanied with a recommendation to take coenzyme Q10, because if a person is deficient in coenzyme Q10, heart failure is more likely.
Beta-blockers (drugs which slow the heart rate and lower blood pressure) can inhibit coenzyme Q10-dependent enzyme reactions.
The 2nd major use of Coenzyme Q10 would be in the case of congestive heart failure, where it is particularly effective. Its importance to the human heart is illustrated by the fact that the heart may cease to function as coenzyme Q10 levels fall by 75%.
In congestive heart failure, the heart cannot pump efficiently, which slows the flow of blood to the lungs and the rest of the body. The heart can temporarily maintain the blood in several ways. It can enlarge to pump extra blood; it can beat faster; or the ventricular walls can become thicker, which can strengthen the pumping ability.
So how does Coenzyme Q10 work? To better understand this, we need to go back to a term from high school biology that you may have forgotten: adenosine triphosphate, also known as 'ATP'.
ATP, occurring in every cell of your body, serves as a source of energy for many of your body's biochemical processes and represents the reserve energy in your muscles. Your heart for example, being a muscle which is continually in motion, needs a constant supply of ATP. This is where the importance of Coenzyme Q10 comes into play: ATP cannot be produced without Coenzyme Q10. Coenzyme Q10 is the catalyst for the creation of ATP. This means that Coenzyme Q10 plays a vital role in the inner workings of your body and, for obvious reasons, is found in the highest concentration in the heart.
High blood pressure (hypertension):
Preliminary research suggests that CoQ10 causes small decreases in blood pressure (systolic and possibly diastolic). Low blood levels of CoQ10 have been found in people with hypertension, although it is not clear if CoQ10 "deficiency" is a cause of high blood pressure. It is not known what dose is safe or effective. CoQ10 is less commonly used to treat hypertension than it is for other heart conditions such as congestive heart failure. Well-designed long-term research is needed to strengthen this recommendation.
Coenzyme Q10 and Parkinson's disease:
Low levels of natural coenzyme Q-10 have been observed in individuals with muscle-wasting diseases (conditions that result in decreased muscle size and efficiency). Therefore, coenzyme Q-10 is being studied as a possible treatment for conditions, such as Parkinson disease (PD), that affect muscle function. Coenzyme Q-10 possible energy-enhancing effects may prevent the deterioration of muscle activity. Additionally, in animal and human studies, increasing amounts of coenzyme Q-10 also seemed to increase levels of a neurotransmitter known as dopamine. Neurotransmitters are chemicals that carry messages from nerve cells to other cells. Individuals with PD generally have low dopamine levels, so raising dopamine may relieve their PD symptoms. Additionally, coenzyme Q-10 may reduce other factors, such as inflammation and damage by oxygen free radicals, that may cause or worsen PD. Studies are less conclusive, however, for coenzyme Q-10 possible effectiveness for other muscle-wasting conditions such as Huntington disease and muscular dystrophy. While these and similar conditions may have a connection to low coenzyme Q-10 levels, it is not known if the lowered levels of coenzyme Q-10 contribute to the conditions or result from them. Much more research is needed in these areas.
Results of the first placebo-controlled, multi-center clinical trial of the compound coenzyme Q10 suggest that it can slow down disease progression in patients with early-stage Parkinson's disease. While the findings must be confirmed in a larger study, they provide hope that coenzyme Q10 may ultimately provide a new way of treating Parkinson's disease.
The phase II study, led by Clifford Shults, M.D., of the University of California, San Diego (UCSD) School of Medicine, looked at a total of 80 Parkinson's disease patients at 10 centers across the U.S. to determine whether coenzyme Q10 is safe and whether it can slow down the rate of functional decline. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS) and appears in the October 15,
2002 issue of the Archives of Neurology.
"This trial suggests that coenzyme Q10 can slow the rate of deterioration in Parkinson's disease," says Dr. Shults. "However, before the compound is used widely, the results need to be confirmed in a larger group of patients."
The researchers believe that coenzyme Q10 works by improving the function of mitochondria, the 'powerhouses' which produce energy in cells. Coenzyme Q10 is an important link in the chain of chemical reactions which produces this energy. It's also a potent antioxidant - a chemical that "mops up" harmful free radicals generated during normal metabolism. Previous studies carried out by Dr. Shults, Richard Haas, M.D., of UCSD and Flint Beal, M.D., of Cornell University have shown that coenzyme Q10 levels in mitochondria in Parkinson's disease patients are reduced and that mitochondrial function in these patients is impaired.
Animal studies have shown that coenzyme Q10 can protect the area of the brain which is damaged in Parkinson's disease. Dr. Shults and his colleagues also conducted a pilot study with Parkinson's disease patients which showed that consumption of up to 800 mg/day of coenzyme Q10 was well tolerated and significantly increased the level of coenzyme Q10 in the bloodstream.
However, in terms of Parkinson's disease, prevention is clearly the best option. The single best thing one can do is avoid pesticide and insecticide exposure.
Coenzyme Q10 and exercise performance Basic biochemistry:
Coenzyme Q10 and related ubiquinones were first discovered in 1955 by RA Morton and associates in Liverpool, England. F.L. Crane and colleagues extracted and isolated ubiquinone from mitochondria and dubbed the term coenzyme Q.The number of side chain isoprenoid units determines the nomenclature. Coenzyme Q6 is found in bacteria whereas CoQ10 is found in mammalian mitochondria. CoQ10 is one part of complex series of reactions that occur within mitochondria -- ultimately linked to the generation of energy within a cell.
With virtually all cofactors and vitamins, deficiency results in poor athletic performance and/or disease. However, in a population of healthy, exercising adults in the U.S. it is rare to find vitamin deficiencies. The concept that, "more vitamin intake will improve performance" has been around a long time. It seems that every time a new factor or biochemical mechanism is discovered, a new product quickly finds its way to the store shelves. Coenzyme Q10 (Co Q10) is one of several important mitochondrial enzymes required for electron transport, and is thus a critical part of the process of generating energy within cells. Supplementation with Co Q10 has occurred for over a decade, despite the lack of firm evidence to support its role a reputed performance enhancer.
To investigate the effects of Co Q10 supplementation it is necessary to look at some of the scientific literature published over the past 10 years. The studies differ in their methods and type of athlete being studied, but all have small sample sizes. These small numbers limit the power of these studies and make far reaching conclusions difficult. Additionally, the studies don¡¯t always agree.
A 1997 study from Finland, which looked at 25 elite cross-country skiers, found significant improvement in physical performance and subjective impressions of the quality of training. Although the results of this study look good,almost too good to be true,there are a few points to consider. First, although it was a placebo controlled trial no effort was made to determine if the skiers were able to tell placebo from the "real" supplement. More rigorous studies often include a post-test questionnaire, because the results of any study will be greatly influenced if athletes are able to identify the placebo and the test supplement. In this study the athletes' performance dropped on placebo versus baseline exercise testing. Placebo should make no difference, unless the athletes' figured out it was placebo. A second point is that other studies have failed to demonstrate performance enhancement with Co Q10.
A 1999 study looked at supplementation with Co Q10, vitamin E, and vitamin C. For the seven well trained male triathletes examined there was no change in VO2 max, muscle energy metabolism, or muscle fatigue in the supplement group versus placebo. Another study from 1996 looked at untrained middle-aged men and found no improvement in exercise capacity with Co Q10 supplementation, although the supplemented group felt more "vigorous". Finally, going back to 1992, a study sponsored by a company that sells a "coenzyme athletic performance system" -- consisting of Co Q10, vitamin E, cytochrome C, and inosine ¨C tested 11 highly trained male triathletes. This study used an interesting exhaustive performance test, which consisted of 90 minutes of treadmill running (70% VO2 max) followed by cycling (70% VO2 max) until exhaustion. Much to the company's dismay there were no benefits versus placebo. Not surprisingly, the company has criticized this study as "flawed".
What are the principal uses of CoQ10(Co Q 10)?
CoQ10 supplementation is used primarily in the treatment of cardiovascular diseases such as elevated cholesterol levels, high blood pressure, congestive heart failure, cardiomyopathy, mitral valve prolapse, coronary artery bypass surgery, and angina. Considerable scientific studies have validated these uses. CoQ10 has also been shown to be helpful in diabetes; periodontal disease; immune deficiency; cancer; as a weight-loss aid; and muscular dystrophy. Since the response of CoQ10 can take time, a noticeable improvement might not occur until 8 or more weeks after therapy is begun.
Several clinical trials and case series have provided evidence, supporting the use of CoQ10 in the prevention and treatment of various disorders related to oxidative stress. (Table 1) It has been shown that CoQ10's antioxidant properties and central role in mitochondrial oxidative phosphorylation make it useful as adjunct therapy for cardiovascular diseases such as CHF, hypertension, stable angina, drug-induced cardiotoxicity, and ventricular arrhythmia, and non-cardiac conditions including cancer, periodontal disease, compromised immune systems, COPD, and muscular dystrophy. Therefore, healthcare professionals are advocating its use as a supplement.
 Alzheimer's disease:
Promising preliminary evidence from human research suggests that CoQ10 supplements may slow down, but not cure, dementia in people with Alzheimer's disease. Additional well-designed studies are needed to confirm this result before a firm recommendation can be made.
Angina (chest pain from clogged heart arteries):
Preliminary small human studies suggest that CoQ10 may reduce angina and improve exercise tolerance in people with clogged heart arteries. Better studies are needed before a firm recommendation can be made.
Anthracycline chemotherapy heart toxicity:
Anthracycline chemotherapy drugs, such as doxorubicin (Adriamycin?), are commonly used to treat cancers such as breast cancer or lymphoma. Heart damage (cardiomyopathy) is a major concern with the use of anthracyclines, and CoQ10 has been suggested to protect the heart. However, studies in this area are small and not high quality and the effects of CoQ10 remain unclear.
Breast cancer:
Several studies in women with breast cancer report reduced levels of CoQ10 in diseased breast tissue or blood. It has been suggested by some researchers that raising CoQ10 levels with supplements might be helpful. However, it is not clear if CoQ10 is beneficial in these patients, or if the low levels of CoQ10 may actually be a part of the body's natural response to cancer, helping to fight disease. Supplementation with CoQ10 has not been proven to reduce cancer, and has not been compared to other forms of treatment for breast cancer.
Studies of women with breast cancer suggest that CoQ10 supplements (in addition to conventional treatment and a nutritional regimen including other antioxidants and essential fatty acids) may shrink tumors, reduce pain associated with the condition, and cause partial remission in some individuals. It is important to recognize that the beneficial effects these women experienced cannot be attributed to CoQ10 alone. Additional antioxidants used in these studies include vitamins C, E, and selenium.
Cardiomyopathy (dilated, hypertrophic):
CoQ10 may also help people with some forms of cardiomyopathy. Patients should consult their physician about the possible benefits of supplementation for this condition.There is conflicting evidence from research on the use of CoQ10 in patients with dilated or hypertrophic cardiomyopathy. Different levels of disease severity have been studied (New York Heart Association heart failure classes I through IV). Some studies report improved heart function (ejection fraction, stroke volume, cardiac index, exercise tolerance), while others find no improvements. Most trials are small or not well designed. Better research is needed in this area before a recommendation can be made.
Congestive Heart Failure (CHF):
Levels of CoQ10 are low in people with CHF, a debilitating disease that occurs when the heart is not able to pump blood effectively. This can cause blood to pool in parts of the body such as the lungs and legs. Information from many research studies suggests that CoQ10 supplements help reduce swelling in the legs, enhance breathing by reducing fluid in the lungs, and increase exercise capacity in people with CHF. Not all studies agree, however. As a result, some experts conclude that CoQ10 supplements do not contribute any benefit to the usual conventional treatment for CHF. More conclusive research will help resolve the debate.
Diabetes:
Preliminary evidence suggests that CoQ10 does not affect blood sugar levels in patients with type 1 or type 2 diabetes, and does not alter the need for diabetes medications.
CoQ10 supplements may improve heart health and blood sugar and help manage high cholesterol and high blood pressure in individuals with diabetes. (High blood pressure, high cholesterol, and heart disease are all common problems associated with diabetes). Despite some concern that CoQ10 may cause a sudden and dramatic drop in blood sugar (called hypoglycemia), two recent studies of people with diabetes given CoQ10 two times per day showed no hypoglycemic response. The safest bet if you have diabetes is to talk to your doctor or registered dietitian about the possible use of CoQ10.
Exercise performance:
The effects of CoQ10 on exercise performance have been tested in athletes, normal healthy individuals, and in people with chronic lung disease. Results are variable, with some research suggesting benefits, and other studies showing no effects. Most trials have not been well-designed. Better research is necessary before a firm conclusion can be drawn.
Friedreich's ataxia:
Preliminary research reports promising evidence for the use of CQ10 in the treatment of Friedreich's ataxia. Further evidence is necessary before a firm conclusion can be drawn.
Gum disease (periodontitis):
Preliminary human studies suggest possible benefits of CoQ10 taken by mouth or placed on the skin or gums in the treatment of periodontitis. Improvements in bleeding, swelling, and pain are reported. However, available studies are small and not high quality. Better research is needed before a conclusion can be drawn.
Heart Disease:
Researchers believe that the beneficial effect of CoQ10 in the prevention and treatment of heart disease is due to its ability to improve energy production in cells, inhibit blood clot formation, and act as an antioxidant. One important study, for example, found that people who received daily CoQ10 supplements within 3 days of a heart attack were significantly less likely to experience subsequent heart attacks and chest pain. In addition, these same patients were less likely to die of heart disease than those who did not receive the supplements.
Heart attack (acute myocardial infarction):
There is preliminary human study of CoQ10 given to patients within three days after a heart attack. Reductions in deaths, abnormal heart rhythms, and second heart attacks are reported, although better research is needed before a firm conclusion can be drawn.
Heart failure:
The evidence for CoQ10 in the treatment of heart failure is controversial and remains unclear. Different levels of disease severity have been studied (New York Heart Association classes I through IV). Several studies have shown benefits of coenzyme Q10 in people who have been diagnosed with chronic heart failure (with or without cardiomyopathy), including in transplant recipients. Some studies report improved heart function (ejection fraction, stroke volume, cardiac index, exercise tolerance), while others find no improvements. Most trials are small or not well designed. In some parts of Europe, Russia, CoQ10 is considered a part of standard therapy for congestive heart failure patients. Better research is needed in this area, studying effects on quality of life, hospitalization, death rates, before a recommendation can be made. C
Based on results from several studies, coenzyme Q-10 appears to be safe for helping to treat heart diseases in individuals with diabetes; but whether it affects blood sugar levels is not known conclusively. Results from some studies may show a small decrease in blood sugar levels when coenzyme Q-10 is taken by individuals with diabetes, but other studies have found no effects on insulin production or utilization. Coenzyme Q-10 may be slightly effective for individuals with an inherited type of diabetes known as maternally inherited diabetes mellitus and deafness (MIDD).
Heart protection during surgery:
Several studies suggest that the function of the heart may be improved after major heart surgeries such as coronary artery bypass graft (CABG) or valve replacement when CoQ10 is given to patients before or during surgery. Better studies that measure effects on long-term heart function and survival are necessary before a recommendation can be made.
Heart Surgery:
Research indicates that introducing CoQ10 prior to heart surgery, including bypass surgery and heart transplantation, can reduce damage caused by free radicals, strengthen heart function, and lower the incidence of irregular heart beat (arrhythmias) during the recovery phase.
High Blood Pressure:
Several studies involving small numbers of people suggest that CoQ10 may lower blood pressure. However, it may take 4 to 12 weeks before any beneficial effect is observed. More research with greater numbers of people is needed to assess the value of CoQ10 in the treatment of high blood pressure.
High Cholesterol:
Levels of CoQ10 tend to be lower in people with high cholesterol compared to healthy individuals of the same age. In addition, certain cholesterol-lowering drugs called statins (such as atorvastatin, cerivastatin, lovastatin, pravastatin, simvastatin) appear to deplete natural levels of CoQ10 in the body. Taking CoQ10 supplements can correct the deficiency caused by statin medications without affecting the medication's positive effects on cholesterol levels.
HIV/AIDS:
There is limited evidence that natural levels of CoQ10 in the body may be reduced in people with HIV/AIDS. There is no reliable scientific research showing that CoQ10 supplements have any effect on this disease. C
Mitochondrial diseases and Kearns-Sayre syndrome:
COQ10(Co Q 10) is often recommended for patients with mitochondrial diseases, including myopathies, encephalomyopathies, and Kearns-Sayre syndrome. Several early studies report improvements in metabolism and physical endurance in patients with these conditions after treatment with CoQ10, although most available research is not high quality or definitive. Better studies are needed before a strong recommendation can be made. C
Muscular dystrophies:
Preliminary studies in patients with muscular dystrophy taking COQ10 supplements describe improvements in exercise capacity, heart function, and overall quality of life. Additional research is needed in this area. C
Summary:Preliminary studies also suggest that CoQ10(Co Q 10) may:
Coenzyme Q10 Improve immune function in individuals with immune deficiencies (such as AIDS) and chronic infections (such as yeast and other viral infections).
Coenzyme Q10 Increase sperm motility leading to enhanced fertility.
Coenzyme Q10 Be used as part of the treatment for Alzheimer's disease.
Coenzyme Q10 Reduce damage from stroke.
Coenzyme Q10 Boost athletic performance.
Coenzyme Q10 Enhance physical activity in people with fatigue syndromes.
Coenzyme Q10 Improve exercise tolerance in individuals with muscular dystrophy.
Coenzyme Q10 is a fat-soluble compound primarily synthesized by the body and also consumed in the diet.
Coenzyme Q10 is required for mitochondrial ATP synthesis and functions as an antioxidant in cell membranes and lipoproteins.
Endogenous synthesis and dietary intake appear to provide sufficient coenzyme Q10 to prevent deficiency in healthy people.
Oral supplementation of coenzyme Q10 increases plasma, lipoprotein, and blood vessel levels, but it is unclear whether tissue coenzyme Q10 levels are increased, especially in healthy individuals.
Coenzyme Q10 supplementation has resulted in clinical and metabolic improvement in some patients with hereditary mitochondrial disorders.
Although coenzyme Q10 supplementation may be a useful adjunct to conventional medical therapy for congestive heart failure, additional research is needed.
Roles for coenzyme Q10 supplementation in other cardiovascular diseases, neurodegenerative diseases, cancer, and diabetes require further research.
Coenzyme Q10 supplementation does not appear to improve athletic performance.
Although coenzyme Q10 supplements are relatively safe, they may decrease the anticoagulant efficacy of warfarin (Coumadin).
Presently, it is unclear whether individuals taking cholesterol-lowering medications, known as HMG-CoA reductase inhibitors (statins), would benefit from coenzyme Q10
Uses based on tradition or theory:Amyotrophic lateral sclerosis (ALS), antioxidant, asthma, Bell's palsy, breathing difficulties, cancer, cerebellar ataxia, chronic fatigue syndrome, chronic obstructive pulmonary disease (COPD), deafness, decreased sperm motility (idiopathic asthenozoospermia), gingivitis, hair loss (and hair loss from chemotherapy), heart irregular beats, hepatitis B, high cholesterol, Huntington's chorea/disease, immune system diseases, infertility, insomnia, kidney failure, leg swelling (edema), life extension, liver enlargement or disease, lung cancer, lung disease, macular degeneration, MELAS syndrome, MIDD (maternally inherited diabetes mellitus and deafness), mitral valve prolapse, nutrition, obesity, Papillon-Lefevre Syndrome, Parkinson's disease,physical performance, prevention of muscle damage from "statin" cholesterol-lowering drugs, psychiatric disorders, QT-interval shortening; reduction of phenothiazine drug side effects, reduction of tricyclic antidepressant (TCA) drug side effects, stomach ulcer.
Actions and Pharmacology for CoQ10(Co Q 10).:
Actions:Supplemental CoQ10 may have cardioprotective, cytoprotective and neuroprotective activities:
Mechanism of Action:
Electron Transport Chain to Produce ATP: CoQ10, found in the inner mitochondrial membrane, is the cofactor for at least three mitochondrial enzymes (complexes I, II and III) that play a vital role in oxidative phosphorylation. It functions as the only non-protein component of the electron transport chain (ETC) in addition to not being attached to a protein itself. This unique characteristic enables CoQ10 to move and transfer electrons between flavoproteins and cytochromes. Each pair of electrons processed by the ETC must first interact with CoQ10, which is considered the central rate-limiting constituent of the mitochondrial respiratory chain. Therefore, CoQ10 plays an essential role in adenosine triphosphate (ATP), or biological energy, production.
Since the actions of supplemental CoQ10 have yet to be clarified, the mechanism of these actions is a matter of speculation. However, much is known about the biochemistry of CoQ10. CoQ10 is an essential cofactor in the mitochondrial electron transport chain, where it accepts electrons from complex I and II, an activity that is vital for the production of ATP.
CoQ10 has antioxidant activity in mitochondria and cellular membranes, protecting against peroxidation of lipid membranes. It also inhibits the oxidation of LDL-cholesterol. LDL-cholesterol oxidation is believed to play a significant role in the pathogenesis of atherosclerosis.
CoQ10 is biosynthesized in the body and shares a common synthetic pathway with cholesterol. CoQ10 levels decrease with aging in humans. Why this occurs is not known but may be due to decreased synthesis and/or increased lipid peroxidation which occurs with aging.
Membrane Stabilization and Fluidity:
The membrane stabilizing property of CoQ10 has been postulated to involve the phospholipid-protein interaction that increases prostaglandin (especially prostacyclin) metabolism. It is thought that CoQ10 stabilizes myocardial calcium-dependent ion channels and prevents the depletion of metabolites essential for ATP synthesis. CoQ10 also decreases blood viscosity, and improves blood flow to cardiac muscle in patients with ischemic heart disease.
Pharmacokinetics and Clinical uses Overview:
CoQ10 is absorbed from the small intestine into the lymphatics; from there it enters the blood. Absorption of CoQ10 is poor. Well over 60% of an oral dose is excreted in the feces. Furthermore, absorption of CoQ10 is highly variable and depends not only on food intake but also on the amount of lipids present in the food. Absorption is lower on an empty stomach and greater when taken with food of high lipid content. In the blood, CoQ10 is partitioned into the various lipoprotein particles, including VLDL, LDL and HDL.
;It takes about three weeks of daily dosing with CoQ10 to reach maximal serum concentrations, which then plateau with continuous daily dosing. CoQ10 is distributed to the various tissues of the body and is able to enter the brain. The main elimination of CoQ10 occurs via bile.
Congestive Heart Failure (CHF):
Several open and controlled studies have examined the efficacy of CoQ10 as adjunctive therapy for treating CHF. The presence of increasing symptoms associated with CHF has been correlated to the severity of CoQ10 deficiency. In one study, the mean myocardial tissue level (dry weight) of CoQ10 from endomyocardial biopsies obtained during catheterization in control subjects, New York Heart Association (NYHA) Class I with normal hemodynamic findings and normal biopsy morphology, were compared to that of NYHA Functional Class III or IV patients; these levels were reported as 0.42 and 0.28, respectively. The authors concluded that CoQ10 myocardial tissue levels in CHF patients are on average 33% lower than in control patients. The degree of CoQ10 deficiency correlated with the severity of symptoms and presence of dilated cardiomyopathy in NYHA Class III and IV patients. Study by Jameson et al. analyzed serum CoQ10, alpha-tocopherol, and free cholesterol levels in 94 consecutive hospitalized patients over 50 years of age. Patients exhibiting a significantly lower serum free cholesterol-related CoQ10 value (CoQ10 levels expressed per milligram of free cholesterol) had an increased risk of CHF, severe myalgia, concomitant use of cytostatic and lipid-lowering drug therapy, and/or death within a six-month follow-up.
Myocardial infarction and cardiac surgery:
The heart muscle may become oxygen-deprived (ischemic) as the result of myocardial infarction (MI) or during cardiac surgery. Increased generation of ROS when the heart muscle's oxygen supply is restored (reperfusion) is thought to be an important contributor to myocardial damage occurring during ischemia-reperfusion. Pretreatment of animals with coenzyme Q10 has been found to decrease myocardial damage due to ischemia-reperfusion. Another potential source of ischemia-reperfusion injury is aortic clamping during some types of cardiac surgery, such as coronary artery bypass graft (CABG) surgery. Three out of 4 placebo-controlled trials found that coenzyme Q10 pretreatment (60-300 mg/d 7-14 days prior to surgery) provided some benefit in short-term outcome measures after CABG surgery. In the placebo-controlled trial that did not find preoperative coenzyme Q10 supplementation to be of benefit, patients were treated with 600 mg of coenzyme Q10 twelve hours prior to surgery, suggesting that preoperative coenzyme Q10 treatment may need to commence at least one week prior to CABG surgery in order to realize any benefit. Although the results are promising, these trials have included relatively few people and have only examined outcomes shortly after CABG surgery.
Hypertension:
The results of several small, uncontrolled studies in humans suggest that coenzyme Q10 supplementation could be beneficial in the treatment of hypertension. More recently, two short-term placebo-controlled trials found that coenzyme Q10 supplementation resulted in moderate blood pressure decreases in hypertensive individuals. The addition of 120 mg/d of coenzyme Q10 to conventional medical therapy for 8 weeks in patients with hypertension and coronary artery disease decreased systolic blood pressure by an average of 12 mm Hg and diastolic blood pressure by an average of 6 mm Hg compared to a placebo containing B-complex vitamins. In patients with isolated systolic hypertension, supplementation with 120 mg/d of coenzyme Q10 and 300 IU/day of vitamin E for 12 weeks resulted in an average decrease of 17 mm Hg in systolic blood pressure compared with 300 IU/day of vitamin E alone. Further research is needed to determine whether coenzyme Q10 supplementation can provide significant long-term benefit in the treatment of hypertension.
Diabetes mellitus:
Diabetes mellitus is a condition of increased oxidative stress and impaired energy metabolism. Plasma levels of reduced coenzyme Q10 (CoQH2) have been found to be lower in diabetic patients than healthy controls when normalized to plasma cholesterol levels. However, supplementation with 100 mg/d of coenzyme Q10 for 3 months neither improved glycemic (blood glucose) control nor decreased insulin requirements in Type 1 (insulin-dependent) diabetics compared to placebo. Similarly, 200 mg/d of coenzyme Q10 supplementation for 6 months did not improve glycemic control or serum lipid profiles in Type 2 (non-insulin dependent) diabetics. Since coenzyme Q10 supplementation did not interfere with glycemic control in either study, the authors of both studies concluded that coenzyme Q10 supplements could be used safely in diabetic patients as adjunct therapy for cardiovascular diseases.
Cancer:
Numerous studies have noted the incidence of CoQ10 deficiency in a variety of cancers including breast, lung, prostate, pancreatic and colon cancer. In an open-label study of 32 breast cancer patients with metastases to axillary lymph nodes, 90 mg/day of CoQ10 plus high-dose antioxidant therapy with vitamin C, vitamin E, beta carotene, selenium, and omega-3 and omega-6 fatty acids were given in addition to conventional surgery and chemotherapy. During the 18-month study period, none of the patients showed signs of further metastases and six of the 32 patients had partial tumor regression.
Immune Modulation:
Studies have demonstrated that the degree of CoQ10 deficiency is correlated with the severity of immune compromised diseases. Patients with acquired immune deficiency syndrome (AIDS) showed statistically significant lower CoQ10 serum concentrations than AIDS-related complex (ARC) patients, who in turn had lower levels than healthy subjects. 31 A clinical case series of eight adult patients treated with 60 mg/day of CoQ10 reported significant increases in serum IgG levels over 1¨C4 months.
Neurodegenerative Diseases:
Parkinson's disease: Parkinson's disease is a degenerative neurological disorder characterized by tremors, muscular rigidity, and slow movements. It is estimated to affect approximately 1% of Americans over the age of 65. Although the causes of Parkinson's disease are not all known, decreased activity of complex I of the mitochondrial electron transport chain and increased oxidative stress in a part of the brain called the substantia nigra are thought to play a role. Coenzyme Q10 is the electron acceptor for complex I as well as an antioxidant, and decreased ratios of reduced to oxidized coenzyme Q10 have been found in platelets of individuals with Parkinson's disease. A 16-month randomized placebo-controlled trial evaluated the safety and efficacy of 300, 600, or 1200 mg/d of coenzyme Q10 in 80 people with early Parkinson's disease. Coenzyme Q10 supplementation was well tolerated at all doses and associated with slower deterioration of function in Parkinson's disease patients compared to placebo. However, the difference was statistically significant only in the group taking 1200 mg/d. Although these preliminary findings are promising, they need to be confirmed in larger clinical trials before recommending the use of coenzyme Q10 in early Parkinson's disease.
Huntington's disease: Huntington's disease is an inherited neurodegenerative disorder characterized by selective degeneration of nerve cells known as striatal spiny neurons. Symptoms, such as movement disorders and impaired cognitive function, typically develop in the fourth decade of life and progressively deteriorate over time. Animal models indicate that impaired mitochondrial function and glutamate-mediated neurotoxicity may play roles in the pathology of Huntington's disease. Coenzyme Q10 supplementation has been found to decrease brain lesion size in animal models of Huntington's disease and to decrease brain lactate levels in Huntington's disease patients. However, feeding transgenic mice that express the Huntington's disease protein a combination of coenzyme Q10 and remacemide resulted in only transiently improved motor performance and did not prolong survival. 37 Remacemide is an antagonist of the neuronal receptor that is activated by glutamate. A 30-month randomized placebo-controlled trial of coenzyme Q10 (600 mg/d), remacemide, or both in 347 patients with early Huntington's disease found that neither coenzyme Q10 nor remacemide significantly altered the decline in total functional capacity, although coenzyme Q10 supplementation (with or without remacemide) resulted in a nonsignificant 13% decrease in the decline.( 38 ) Currently, there is insufficient evidence to support a recommendation for coenzyme Q10 supplementation in early Huntington's disease.
Coenzyme Q10 in food:
Where is Coenzyme Q10 found? Coenzyme Q10 is primarily found in fish and meat. Our bodies are able to produce some of the CoQ10 that we need. The rest is synthesized from the foods we eat. The highest dietary sources of Coenzyme Q10 come from - in descending order according to content - fresh sardines and mackerel, the heart, liver and meat of beef, lamb and pork along with eggs. There are plenty of vegetable sources of Coenzyme Q10, the richest being spinach, broccoli, peanuts, wheat germ and whole grains - in that order, although the amount is significantly smaller than that found in meats. Also, it is important to note that these foods must be raw, fresh and unprocessed - no milling, canning, preserving, freezing, etc., plus grown/produced in an unpolluted environment to be considered viable sources.
Food products are a good source of CoQ10, and provide approximately half of the body's requirement. Cold-water fish such as mackerel, salmon, sardines, and tuna are particularly high in CoQ10. Vegetable oils and meats also provide good sources. The liver manufactures adequate amounts to fulfill the need not met in the diet. People who are deficient in B vitamins, selenium, vitamin C, and vitamin E may not be able to make as much CoQ10 as they need because these nutrients are required for production. Consumption of foods rich in CoQ10 and production of the nutrient in the liver will not provide the amounts needed to treat heart failure and other conditions that may contribute to a deficiency of this nutrient. In those cases, supplements are required.
Coenzyme Q10 Deficiency:
Normal production of coenzyme Q-10 by humans is highest at about 20 years of age and then it declines gradually. Deficiencies of coenzyme Q-10 are rare, but they result in serious symptoms that include fatigue, muscle weakness, and seizures. Smoking cigarettes reduces the amounts of coenzyme Q-10 in the body, and taking certain drugs such as doxorubicin, some beta-blockers, or certain statins may also lower coenzyme Q-10 levels. Low levels of coenzyme Q-10 are associated with conditions ranging from AIDS and some cancers to periodontal disease. Generally, the extent of coenzyme Q-10 deficiency seems to correlate to the severity of the condition. That is, conditions affected by coenzyme Q-10 levels seem to worsen as coenzyme Q-10 decreases.
Athletes sometimes take supplemental coenzyme Q-10 in the belief that it may increase their ability to perform extended exercise, but study evidence has failed to support this belief.
Normal blood and tissue levels of CoQ10 have been well established by numerous investigators around the world. Significantly decreased levels of CoQ10 have been noted in a wide variety of diseases in both animal and human studies. Insufficient dietary CoQ10, impairment in CoQ10 biosynthesis, excessive utilization of CoQ10 by the body, or any combination of the three, may cause CoQ10 deficiency. Decreased dietary intake is presumed in chronic malnutrition and cachexia.
The relative contribution of CoQ10 biosynthesis versus dietary CoQ10 is under investigation. Karl Folkers takes the position that the dominant source of CoQ10 in man is biosynthesis. This complex, 17-step process, 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, is, by its nature, highly vulnerable. Karl Folkers argues that suboptimal nutrient intake in man is almost universal and that there is subsequent secondary impairment in CoQ10 biosynthesis. This would mean that average or ¡°normal¡± levels of CoQ10 are really suboptimal and the very low levels observed in advanced disease states represent only the tip of a deficiency ¡°ice berg¡±.
HMG-CoA reductase inhibitors used to treat elevated blood cholesterol levels by blocking cholesterol biosynthesis also block CoQ10 biosynthesis. The resulting lowering of blood CoQ10 level is due to the partially shared biosynthetic pathway of CoQ10 and cholesterol. In patients with heart failure this is more than a laboratory observation. It has a significant harmful effect, which can be negated by oral CoQ10 supplementation.
Increased body consumption of CoQ10 is the presumed cause of low blood CoQ10 levels seen in excessive exertion, hypermetabolism, and acute shock states. It is likely that all three mechanisms (insufficient dietary CoQ10, impaired CoQ10 biosynthesis, and excessive utilization of CoQ10) are operable to varying degrees in most cases of observed CoQ10 deficiency.
Patients with certain conditions tend to have lower levels of CoQ10, and may benefit from supplements. Some diseases that are associated with decreased amounts of this nutrient are AIDS, chronic fatigue, congestive heart failure, cardiomyopathy, and inflammatory gum disease. Levels of CoQ10 tend to decrease with age; tests for its presence in the body are not widely available. Adverse effects from this supplement are rare and mild, so anyone suffering from one of the listed conditions should consider discussing supplementation with a health care provider.
Effects of Statin Drugs on CoQ10:
Cholesterol biosynthesis is a complex metabolic process. At least 26 steps are involved in its production, and it shares a common pathway with CoQ10 synthesis. It is produced from acetyl-CoA, just like the isoprenoid side chain of CoQ10. Hydroxymethylglutaryl-coenzyme A (HMG-CoA) is one of the next substrates down the synthesis chain, requiring the enzyme HMG-CoA reductase to form the mevalonate compound.
In the United States, millions of Americans are taking cholesterol-lowering prescription drugs known as "statins" (Pravachol?, Zocor?, Lipitor?, etc.). Statins are a class of pharmaceuticals that are used to lower cholesterol levels, primarily LDL cholesterol. They are sometimes referred to as "HMG-CoA reductase inhibitors," because they block this key enzyme, which is responsible for the body¡¯s production of cholesterol. Essentially, it inhibits the endogenous production of cholesterol.
Inhibition of HMG-CoA reductase by statin drugs at the mevalonate level will inevitably decrease the levels of both cholesterol and CoQ10. The cholesterol-lowering medications interfere with the body's ability to produce CoQ10, because these drugs also block the manufacture of other substances necessary for body functions including CoQ10. Ironically, the drugs are taken to lower cholesterol, but at the same time CoQ10, which protects the heart, is produced on a much smaller scale. People taking statin drugs can develop CoQ10 deficiencies and may require supplementation. Several studies revealed a possible dose-related and significant decrease in CoQ10 serum levels as a result of HMG-CoA reductase inhibitor treatment (e.g., simvastatin, pravastatin, lovastatin) alone. In a double-blind, randomized clinical trial hypercholesterolemic patients received either lovastatin or pravastatin over a period of 18 weeks. At the end of the study period, the total serum level of CoQ10 declined by about 25 percent in the lovastatin and pravastatin groups.
Supplementing with CoQ10 is necessary to prevent its depletion in the body while on these drugs. Furthermore, the LDL cholesterol that is limited by statin drugs is one of the primary transport compounds for CoQ10 in humans. Clearly, statins deliver a double-threat to CoQ10 status through their limitation of production and transport of this important cofactor.
Supplementation and Safety:
CoQ10's safety has been evaluated. Doses of 30-60 mg/day are generally recommended to prevent CoQ10 deficiency and to maintain normal serum concentrations of 0.7-1.0 ug/mL (micrograms per milliliter). However, therapeutic doses of 100-200 mg/day are advocated for the treatment of chronic heart disease. These higher doses may achieve serum concentrations of 2.0-3.0 ug/mL, reported by some investigators to have a positive impact on cardiovascular health. The dosage in a Parkinson¡¯s disease study ranged from 300-1200 mg/day, taken for 16 months. The group that received the largest dose of CoQ10 (1200 mg/day) displayed less of a decline in mental function, motor function, and ability to carry out activities of daily living.
If CoQ10 is going to be effective, adequate blood levels must be maintained for a prolonged period.
CoQ10 is absorbed slowly. Absorption is dependent on the presence of fat in the gastrointestinal (g.i.) tract. Peak plasma levels are attained within 5-10 hours following oral administration. CoQ10 is primarily excreted through the biliary tract, and over 60% of the oral dose is recovered in the feces.
Commercial Production of CoQ10 Supplements:
There are currently two different manufacturing techniques being used to commercially produce coenzyme Q10. the solanesol method and the microbiological fermentation method used. The following is a brief summary of the two manufacturing methods:
The Solanesol Method:
The first CoQ10 to be admitted as a pharmaceutical ingredient was produced by the solanesol method. Plants from the Solanaceae family contain a nine-isoprenoid long alcohol known as solanesol. Solanesol is first extracted from the plant and is then converted to a ten-isoprenoid compound called decaprenol. During the final step, the decaprenol is reacted with hydroquninone to produce CoQ10. The CoQ10 produced by the solanesol method has a long history of safety and efficacy. The compound actually extracted from the tobacco leaf is the solanesol. The process begins with a n-hexane extraction. The solvent is removed by molecular distillation.
With this method, both trans and cis forms of CoQ10 are formed but subsequent purification steps reduce the quantity of cis isomers to below 0.5%, generally below 0.2%.Specification is not more than 0.5%.
Microbiological Fermentation:
Coenzyme Q10 produced by microbiological fermentation was also admitted as a pharmaceutical ingredient nd also has a long history of safety and efficacy. With the fermentation method, selected strains of microbes are placed in a fortified molasses-based carbohydrate medium where they produce CoQ10, as well as CoQ6, CoQ7, CoQ9 and CoQ11 during the fermentation process. The actual microbe used in the process is proprietary. The carbohydrate medium used is derived from sugar beets, but its exact composition is also proprietary.
Subsequent purification steps generally greatly reduce or eliminate the presence of other coenzyme homologues listed above. The USP specification for non-CoQ10 homologues is 1.0%. All of our material meets this requirement. Material produced in this manner is considered natural in the United States, Europe and China. The CoQ10 used is produced by microbiological fermentation, which is the all-trans isomer form.
Recently, there has been a great deal of controversy regarding differences in isomer (cis vs. trans) impurities contained commercially-available products. It is important to note that the compounds involved in the controversy are not hazardous. These impurities are compounds having positive health benefits but the health benefits are not as great as the benefits obtained from all-trans coenzyme Q10.
Coenzyme Q10 manufactured using the solanesol method has the potential to contain "cis" isomers in which the ten-isoprenoid unit tail is bent rather than straight. It is commonly believed that the bent tail limits the molecule's ability to penetrate cellular and organelle membranes. It is also possible that material made using the solanesol method contains some CoQ9. Subsequent purification steps generally greatly reduce or nearly eliminate the presence of these isomers.
Coenzyme Q10 manufactured by microbiological fermentation is 100% in the all-trans isomeric form, identical in structure of the coenzyme Q10 made by the human body. However, material made by microbiological fermentation has the potential to contain other homologues, sometimes referred to "related substances" such as CoQ7, CoQ8, and/or CoQ9. Subsequent purification steps generally greatly reduce or eliminate the presence of the other forms of coenzymes listed above.
All the coenzyme Q10 material utilized is guaranteed to be a minimum of 98% pure. This is considered a natural material and is in full compliance with the current United States Pharmacopeia/ National Formulary (USP/NF), European Pharmacopeia monographs and standards.
Biochemistry of CoQ10:
CoQ10 is made up of a quinone ring, but also contains a side chain consisting of ten repeating 5-carbon isoprene units. Because of its structure, CoQ10 is highly lipophilic and practically insoluble in water. This lipophilic nature also affects bioavailability, making its absorption poor, highly variable, and strongly dependent on the stomach's contents (i.e. foods rich in fat). Another major factor in the bioavailability of CoQ10 is the large size of the molecule. Dietary supplement encapsulators try to develop delivery systems for CoQ10 to enhance bioavailability, and have utilized oil-based soft gel capsules containing microemulsions rather than powder-based forms of this nutrient. However, most CoQ10 dosage forms exhibit negligible dissolution¡ªno more than 10%.
It is clear that the dosage form of a supplement has a significant effect on nutrient bioavailability. Absorption into the general circulation is an important part of delivery. In general, the effect of dosage form on bioavailability depends on the rapidity with which the particular form releases the nutrient into the biological fluids or how rapidly the nutrient may permeate a cell membrane. Not surprisingly, absorption is most rapid from solutions and decreases in the order: solutions, suspensions, capsules, compressed tablets, coated tablets. Commercially available CoQ10 dosage forms include powder-based tablets (compressed), powder-filled capsules (2-piece hard shell), and soft gelatin capsules. Other forms, such as chewable wafers, intra-oral sprays, and intravenous solutions, are available, but are less common.
As previously discussed, the dosage form of a supplement has a significant effect on bioavailability. A prerequisite to absorption is dissolution, and this is a disadvantage of the powder-forms of CoQ10. Better preparations appear to be soft gel capsules with CoQ10 in an oil base, but absorption is still dependent upon the number and size of CoQ10 crystals in the product.
Solubility and Particle Size of Coenzyme Q10 in a Soft Gelatin Formulation:
Coenzyme Q10 (CoQ10) has been characterized as a poorly-soluble, crystalline material. CoQ10 can be rendered soluble in vegetable oils or combinations of vegetable oils and detergent compounds, however re-crystallization has been identified as a challenge to these systems. A citrus-derived monoterpene, d-limonene, was observed to solubilize CoQ10 and this solution was analyzed to confirm solubility.
The solvent:a mixture of d-limonene and tocopherol,was compared with the same solvent mixture plus the addition of CoQ10. These samples were analyzed using visual inspection with a phase contrast microscope at magnifications of 200x, 400x, and 1000x, a dark field microscope, and polarized light microscope. No particles were identified using any of the methods of microscopy.
The samples were also analyzed using a Particle Sizing Systems Nicomp 380 ZLS photon correlation analyzer, a Microtrac UPA 150 Doppler Shift Photon Correlation Analyzer, and a Malvern Zetasizer Nano instrument. Again no particulate material could be detected in either of the samples. The lack of particulate material indicates that CoQ10 can be fully solubilized in a solvent comprised of d-limonene and tocopherol within the concentration limits used in this formulation.
Peak Absorption Study Results:
Starting with day 1 of the study, volunteers took 60 mg CoQsol-CF?, followed by a breakfast consisting of orange juice or milk with a bagel or cereal, and serial blood samples were taken at 0, 4, 6, 8, and 12 hours. Within four hours after ingesting the CoQ10, the plasma levels for the group increased significantly to 1.36 ug/ml. Peak plasma levels occurred at six hours (Tmax) and the maximum plasma concentration (Cmax) was 2.28 ug/ml. Thereafter, plasma CoQ10 rapidly decreased over the next two hours to a mean level of 1.58 ug/ml.
The amount of CoQ10 absorbed at Cmax was 4,769.5 ¦Ìg based on the average plasma volume 3400 ml. When compared to the ingested dose (60,000 ¦Ìg = 60 mg), the percent of the dose absorbed at Cmax is 7.95%. This percentage makes it a superior product in terms of absorption.
Steady State Plasma CoQ10 Bioavailability Results:
Volunteers continued taking 60 mg CoQsol-CF? daily for 28 days. During this time, volunteers followed their regular diet and activity, and returned to the testing facility on days 7, 14, 21, and 28 at 6:00 a.m. in a rested and fasted condition¡ªminimum eight hours for collecting blood samples. The mean plasma-level of CoQ10 were determined and data are shown in the graph. In seven days the mean plasma CoQ10 level increased significantly to 2.39 ug/ml. At the 28th day, the mean plasma CoQ10 was 2.75 ug/ml. This means that in this steady state study, the mean CoQ10 plasma level increased by 200% (calculated increase was 6,458.9 ug/ml at a constant daily dose of 60 mg/day for 28 days).
The area under the plasma CoQ10 and time base curve between days 0 and 28 days (AUC) is used to determine the bioavailability of CoQsol-CF?. The AUC for CoQsol-CF? was 42.27ug/ml.day.
Animal Study
Soft Gel Technologies, Inc.? also funded an animal study on CoQsol-CF? whose main objective was to compare bioavailability and tissue distribution after supplementation with different preparations of CoQ10, including CoQsol-CF?. Previous studies demonstrated that CoQ10 supplementation is associated with increased CoQ accumulation in serum and liver. The significant accumulation of CoQ in tissues other than the liver was also observed but only when high doses of CoQ was administered over longer periods of time. In order to establish whether CoQsol-CF? is superior to powder CoQ10 in terms of enhancing tissue CoQ storage, high daily doses of both formulations are recommended.
Protocol
Young male mice were randomly assigned to 4 groups, 12 animals per group. After acclimation, treatment groups received CoQsol-CF?, CoQsol?, or powder CoQ10 product at the dose 300 mg/kg body weight (BW)/day, by gavage, for 10 weeks. The control group received CoQ10 vehicle (also by gavage) for the same period of time. At the end of the study, blood was collected by heart puncture and tissues were collected. Serum and tissue homogenates (liver, heart, skeletal muscle, spleen, brain and lung) were analyzed for CoQ10, CoQ9, total CoQ and reduced forms of CoQ10 and CoQ9 concentrations by HPLC (high performance liquid chromatography).
Results
It was observed that different preparations lead to accumulation of CoQ in different organs. The graphs depicted below illustrate that various CoQ10 delivery systems accumulate in different tissue types. CoQsol-CF? demonstrated enhanced accumulation in blood serum, heart, and liver tissue, all of which are key storage and use locations for CoQ. Supplementation with our original CoQsol? formula resulted in the accumulation of total CoQ in mitochondria isolated from heart, brain and spleen. Even the CoQ10 powder showed enhanced uptake in muscle and lung tissue. The results of the present study suggest that different preparations are metabolized in different ways leading to the differences observed in tissue accumulation.
Limitations of Animal Study
The mouse is a challenging model for CoQ10 research, because rodents' primary storage form of CoQ is CoQ9. Lipid metabolism differs from humans in that the major source of cholesterol in rodents is from HDL (85-90%), whereas humans obtain cholesterol from LDL. In addition, high serum levels of CoQ in mice may significantly reduce blood pressure, thereby causing a negative response. Despite these limitations, the mouse model provided useful insight for future work.
Design:
A randomized, multi-center, parallel study comparing the bioavailabilities of two coenzyme Q10 formulations (CoQsol-CF? and CoQ10 powder in hard shell capsules) in 30 healthy, human subjects has been initiated. Steady state and acute dose bioavailability in plasma and tissues will be investigated. Antioxidant properties of the two coenzyme Q10 preparations will also be compared. The values studied will include: total antioxidant status, total plasma glutathione, and isoprostane lipid peroxide levels. Functional measures of cardiovascular health including homocysteine and CRP levels will also be measured. In addition, safety data will be gathered.
Indications and Usage:
Coenzyme Q10 may be indicated in cardiovascular disease, particularly in congestive heart failure. It may also be indicated to correct reduced blood levels of CoQ10 that result from the use of HMG-CoA reductase inhibitors used to treat elevated cholesterol levels. It also appears to have usefulness in the management of periodontal disease in some. There is far less evidence to support claims that it has positive effects in cancer, muscular dystrophy and immune dysfunction. Similarly, there is as yet no reliable evidence that it can inhibit obesity or enhance athletic performance.
Chemistry/function: The primary biochemical action of CoQ10 is as a cofactor in the electron-transport chain, a series of oxidation-reduction reactions involved in cellular respiration and the synthesis of ATP. CoQ10 can be synthesized in vivo. However, in some situations the need for CoQ10 may surpass the body's ability to synthesize it. CoQ10 is well-absorbed by oral supplementation as evidenced by significant increases in serum CoQ10 levels after supplementation.
Dietary sources: Broccoli, spinach, meat, nuts and fish.
Deficiency: The deficiency pattern associated with coenzyme Q10 has not been clearly defined. A deficiency may result from impaired synthesis due to nutritional deficiencies; genetic or acquired defect in synthesis or utilization; increased tissue needs resulting from illness. CoQ10 levels decline with advancing age and the elderly are known to generally have lower levels of CoQ10. Likewise, researchers have observed that the patient populations exhibiting many of the conditions CoQ10 is used to treat more often demonstrate low levels of CoQ10; these include cardiomyopathy, gingivitis, heart failure, and HIV/AIDS.
Known or potential therapeutic uses: Allergies, angina, arrhythmias, breast cancer, cardiovascular disease, chemotherapy support, congestive heart failure, diabetes mellitus, gingivitis, HIV/AIDS support, hypertension, male infertility, mitral valve prolapse, muscular dystrophy, obesity, periodontal disease. Supplementation may also enhance aerobic capacity and muscle performance, especially in sedentary individuals.
Research Summary:
There are many studies, spanning more than two decades, reporting positive results from the use of CoQ10 as adjunctive therapy in the treatment of congestive heart failure. CoQ10 has been an approved drug for use in congestive heart failure since 1974. It has also been approved for this use in some other countries. Several studies have demonstrated a strong correlation between severity of heart disease and severity of CoQ10 deficiency. Some have suggested that this deficiency is the primary cause of some variations of heart muscle dysfunction, while others believe it plays a secondary role in the etiology of heart failure.
Early studies of congestive heart failure focused on idiopathic dilated cardiomyopathy, testing CoQ10 against placebo using echocardiography to assess heart function. Echocardiographic improvement seen in these studies was generally slow but sustained and was accompanied by diminished fatigue, chest pain, dyspnea and palpitations. Normal heart size and function were restored in some patients using only CoQ10; this occurred primarily in patients with recent onset of congestive heart failure.
Subsequently, nearly all of the several placebo-controlled studies investigating CoQ10's effects on heart muscle function have reported significant positive results. One multi-center Italian study included 2,664 patients with congestive heart failure. No notable adverse effects on drug interactions have been reported in these studies except for one report that noted a slight diminution in coumadin activity.
Many studies to date have examined CoQ10 as an addition to standard medical treatments. In several studies involving hypertension and other manifestations of cardiovascular disease, there was a significant reduction in the use of concomitant drug therapies when CoQ10 was added to the treatment regimen.
It is now known that the HMG-CoA reductase inhibitors, while very effective in lowering cholesterol levels, also significantly lower levels of CoQ10. This may be particularly hazardous for patients with heart failure, suggesting a possible indication for CoQ10 in many, if not all, individuals using these cholesterol-lowering drugs. There has been some suggestion that CoQ10, especially if it could be more readily absorbed, might be a cholesterol-lowering agent itself. There is, however, no evidence for this.
Significant CoQ10 deficiencies have been noted in diseased gingiva. CoQ10's efficacy in reducing gingival inflammation and periodontal pocket-depth has been demonstrated in placebo-controlled trials. Claims that CoQ10 might be an effective anti-cancer agent are based upon a few suggestive case histories that will require far more rigorous clinical investigation before these claims can be properly evaluated. Similarly, claims that CoQ10 might be useful in AIDS and some other immune dysfunctions are premature.
It is not unreasonable to hypothesize that CoQ10 might be helpful in muscular dystrophy,and there is some very preliminary animal and clinical data suggesting that it might be. Muscular dystrophy is usually associated with cardiac disease. Research is ongoing but, to date, is inconclusive.
There is also some evidence that CoQ10 might boost energy and speed recovery of exercise-related muscle exhaustion and damage. This work, too, needs more rigorous followup.
There is no evidence that CoQ10 can inhibit obesity.
Warnings and Precautions:
There is one report of CoQ10 decreasing the effectiveness of warfarin. Those taking warfarin should be aware of this possibility.
Because of lack of long-term safety studies, pregnant women and nursing mothers should avoid CoQ10 supplements.
Clinical reports suggest that supplemental CoQ10 may improve beta-cell function and glycemic control in type II diabetics. CoQ10 does not appear to improve glycemic control in type I diabetics. Diabetics should be made aware of this possibility, and those diabetics who do use supplemental CoQ10 should determine by appropriate monitoring if they need to make any adjustments in their diabetic medications.
As of 2004, the safety of CoQ10 for pregnant or breast-feeding women has not been established, and its use is not recommended under these conditions. It is also not recommended for young children. People diagnosed with heart failure, diabetes, kidney problems, or liver disease should use particular care with this supplement, as the dosage of other medications may require adjustment. These individuals should consult a physician before taking coenzyme Q10.
Results from a recent small study done in Italy suggest that coenzyme Q-10 may pass from a mother to her infant in breast milk, but not in blood before birth. Very little other information is available on how coenzyme Q-10 might affect a developing fetus, an infant, or a small child. Therefore, its use is not recommended during pregnancy, while breast-feeding, or during early childhood.
Individuals with diabetes should avoid using large amounts of coenzyme Q-10 because it can lower blood sugar levels, potentially resulting in hypoglycemia (blood sugar that is too low). Symptoms of low blood sugar include shakiness, sweating, confusion, distorted speech, and loss of muscle control. If not corrected, low blood sugar can lead to unconsciousness and even death.
Adverse Reactions:
Mild gastrointestinal symptoms such as nausea, diarrhea and epigastric distress have been reported, particularly with higher doses (200 milligrams or more daily).
Side effects:
Occasional reports of nausea, anorexia, or skin eruptions have been reported with supplementation of CoQ10. Documented adverse effects associated with the use of CoQ10 in humans have been minor and include epigastric discomfort (0.39%), appetite suppression (0.23%), nausea (0.16%) and diarrhea (0.12%).These complaints are dose-related and minimized with dose reduction and/or dose division. Higher than usual doses exceeding 300 mg/day have been associated with elevated serum LDH and SGOT levels, however no hepatic toxicity has been observed. Late night administration has also been reported to cause insomnia.
There are few serious reported side effects of CoQ10. Side effects are typically mild and brief, stopping without any treatment needed. Reactions may include nausea, vomiting, stomach upset, heartburn, diarrhea, loss of appetite, skin itching, rash, insomnia, headache, dizziness, irritability, increased light sensitivity of the eyes, fatigue, or flu-like symptoms.
CoQ10 may lower blood sugar levels. Caution is advised in patients with diabetes or hypoglycemia, and in those taking drugs, herbs, or supplements that affect blood sugar. Serum glucose levels may need to be monitored by a healthcare provider, and medication adjustments may be necessary.
Low blood platelet number was reported in one person taking CoQ10. However, other factors (viral infection, other medications) may have been responsible. Lowering of platelets may increase the risk of bruising or bleeding, although there are no known reports of bleeding from CoQ10. Caution is advised in people who have bleeding disorders or who are taking drugs that increase the risk of bleeding. Dosing adjustments may be necessary.
CoQ10 may decrease blood pressure, and caution is advised in patients with low blood pressure or taking blood pressure medications. Elevations of liver enzymes have been reported rarely, and caution is advised in people with liver disease or taking medications that may harm the liver. CoQ10 may lower blood levels of cholesterol or triglycerides. Thyroid hormone levels may be altered based on one study.
Organ damage due to lack of oxygen/blood flow during intense exercise has been reported in a study of patients with heart disease, although the specific role of CoQ10 is not clear. Vigorous exercise is often discouraged in people using CoQ10 supplements.
Reported adverse effects related to supplemental CoQ10 use include diarrhea, irritation of the stomach, poor appetite, and nausea. These effects are rarely reported and are mild. CoQ10 is considered extremely safe for most people. If doses over 300 mg per day are taken, liver enzyme levels may be affected, and may need monitoring.
Pregnancy and Breastfeeding: There is not enough scientific evidence to support the safe use of CoQ10 during pregnancy or breastfeeding.
Toxicity: No toxicities have been reported or suspected as being associated with Coenzyme Q10.
Contraindications: None known at this time for healthy individuals. Individuals suffering from congestive heart failure should only discontinue supplementation with CoQ10 under the supervision of their physician.
Interactions with Drugs:
In theory and based on a human case report, coenzyme Q10 may reduce the effectiveness of warfarin (Coumadin?), and may limit or prevent effective anticoagulation (blood "thinning"). CoQ10 may reduce blood pressure and may add to the effects of other blood pressure lowering drugs. In theory, CoQ10 may affect thyroid hormone levels and alter the effects of thyroid drugs such as levothyroxine (Synthroid?), although this has not been proven in humans.
Based on theory and human research, a number of drugs may deplete natural levels of CoQ10 in the body. It has not been shown that there are benefits of CoQ10 supplements in people using these agents.
Examples include: diabetes drugs such as chlorpropamide, glimepiride, glipizide, glyburide, metformin, tolazamide, tolbutamide, acetohexamide; methyldopa; clonidine; gemfibrozil; tricyclic antidepressant drugs such as amitriptyline, clomipramine, doxepin, imipramine, trimipramine; antipsychotic medications such as chlorpromazine, fluphenazine, haloperidol, mesoridazine, prochlorperazine, promethazine, thioridazine, trifluoperazine, trimipramine; beta-blocker drugs such as acebutolol, atenolol, betaxolol, bisoprolol, carvedilol, esmolol, labetalol, metoprolol, nadolol, penbutolol, pindolol, propanolol, sotalol, timolol; HMG-CoA reductase inhibitors ("statins") such as atorvastatin, cerivastatin (no longer available in U.S.), fluvastatin, lovastatin, pravastatin, simvastatin; and diuretic drugs ("water pills") such as benzthiazide, hydralazine, chlorthiazide, hydrochlorothiazide, indapamide, methyclothiazide, metolazone, polythiazide.
Due to its possible blood sugar-lowering effects, coenzyme Q-10 may interfere with insulin and oral drugs for diabetes, such as:
Actos,Avandia,glimepiride (Amaryl),glipizide (Glucotrol XL),glyburide (Glynase),Glyset,metformin (Glucophage),Prandin,Precose.
Due to its potential ability to lower blood pressure, coenzyme Q-10 may increase the effects of drugs that also lower blood pressure. Some blood pressure-lowering drugs are:
ACE inhibitors such as captopril, enalapril, fosinopril, and lisinopril
Beta blockers such as atenolol, metoprolol, and propranolol
Calcium channel blockers such as nifedipine, Norvasc, and verapamil
Diuretics such as Dyazide, furosemide, and hydrochlorothiazide
Because coenzyme Q-10 is similar in structure to vitamin K, which increases the blood's ability to clot, coenzyme Q-10 may interfere with anti-clotting medications such as warfarin or heparin.
Coenzyme Q-10 may increase the effects of dopamine, so taking it may also increase the effectiveness of drugs that increase dopamine. Dopamine-enhancing drugs often are used to treat Parkinson's disease. They include:
bromocriptine (Parlodel),cabergoline (Dostinex),carbidopa-levodopa (Dopar, Sinemet),Mirapex,pergolide,Requip
Taking certain cholesterol-lowering drugs known as HMG Co-A reductase inhibitors or statins, seems to lower coenzyme Q-10 levels in the body. The consequences of this effect are not completely understood, but this interaction may account in part for severe muscle deterioration that is rarely associated with taking statins. Statins thought to affect coenzyme Q-10 include:
lovastatin (Mevacor),pravastatin (Pravachol),simvastatin (Zocor)
Propranolol (Inderal), a drug often used to treat hypertension, and doxorubicin (Adriamycin, Doxil, Rubex), an anticancer drug; may also limit or block the energy-producing activity of coenzyme Q-10.
Warfarin:
There is one report of CoQ10 decreasing the effectiveness of warfarin.Concomitant use of warfarin (Coumadin) and coenzyme Q10 supplements has been reported to decrease the anticoagulant effect of warfarin in at least 4 cases.An individual on warfarin should not begin taking coenzyme Q10 supplements without consulting the health care provider that is managing his or her anticoagulant therapy. If warfarin and coenzyme Q10 are to be used concomitantly, blood tests to assess clotting time (prothrombin time; PT/INR) should be monitored frequently, especially in the first two weeks.
HMG-CoA reductase inhibitors (statins):
HMG-CoA reductase is an enzyme that plays a critical role in the regulation of cholesterol synthesis as well as coenzyme Q10 synthesis, although it is now recognized that there are additional rate-limiting steps in the biosynthesis of cholesterol and coenzyme Q10. HMG-CoA reductase inhibitors, also known as statins, are widely used cholesterol-lowering medications that may also decrease the endogenous synthesis of coenzyme Q10. A number of studies have observed decreases in plasma or serum coenzyme Q10 levels in people on HMG-CoA reductase inhibitor therapy, especially those taking simvastatin (Zocor). In contrast to most earlier studies, a randomized cross-over trial in healthy individuals found no significant changes in serum coenzyme Q10 levels after 4 weeks of pravastatin (Pravachol) and atorvastatin (Lipitor) therapy despite significant decreases in total and LDL-cholesterol levels on both medications. In rats, high doses of lovastatin for 4 weeks decreased blood, liver, and heart concentrations of coenzyme Q. However, it is not clear whether HMG-CoA reductase inhibitor therapy decreases tissue coenzyme Q10 concentrations in humans. Although simvastatin treatment for 6 months |
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