CoQ10 is a fat-soluble vitamin-like substance present in every cell of the body and serves as a coenzyme for several of the key enzymatic steps in the production of energy within the cell. It also functions as an antioxidant which is important in its clinical effects.
It is naturally present in small amounts in a wide variety of foods but is particularly high in organ meats such as heart, liver and kidney, as well as beef, soy oil, sardines, mackerel and peanuts. To put dietary CoQ10 intake into perspective, one pound of sardines, two pounds of beef, or two and one half pounds of peanuts, provide 30mg of CoQ10. CoQ10 is also synthesized in all tissues and in healthy individuals normal levels are maintained both by CoQ10 intake and by the body’s synthesis of CoQ10. It has no known toxicity or side effects.
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. CoQ10 deficiency may be caused by insufficient dietary CoQ10, impairment in CoQ10 biosynthesis, excessive utilization of CoQ10 by the body, or any combination of the three.
Decreased dietary intake is presumed in chronic malnutrition and wasting conditions. The relative contribution of CoQ10 biosynthesis in the human body versus dietary CoQ10 is under investigation. This complex production process requires at least seven vitamins and several trace elements. It is argued 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 “iceberg”.
HMG-CoA reductase inhibitors (all the “statin” drugs) that are used to treat elevated blood cholesterol levels by blocking cholesterol synthesis also block CoQ10 synthesis. The resulting lowering of blood CoQ10 level is due to the partially shared biosynthetic pathway of CoQ10 and cholesterol. In patients with heart failure they have 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.
Internationally, there have been at least nine placebo-controlled studies on the treatment of heart disease with CoQ10. All nine of these studies have confirmed the effectiveness of CoQ10 as well as its remarkable safety. Treatment with CoQ10 significantly improves heart muscle function while producing no adverse effects or drug interactions.
The largest study to date involved 2,664 patients with heart failure. Diastolic dysfunction – one of the earliest identifiable signs of myocardial failure – is often found in mitral valve prolapse, hypertensive heart disease and certain fatigue syndromes. Diastolic dysfunction is seen early in the course of many common cardiac disorders and can be demonstrated by echocardiography. The heart muscle stiffening found here returns towards normal with supplemental CoQ10 along with clinical improvement of symptoms. It is important to note that in all of the above clinical trials, CoQ10 was used in addition to traditional medical treatments, not to their exclusion. Hypertension is reduced when diastolic function improves.
The dosage of CoQ10 used in clinical trials has evolved over the past 20 years. Initially, doses as small as 30-45mg per day were associated with measurable clinical responses in patients with heart failure. Additional studies have used higher doses with improved clinical response, again in patients with heart failure. Some patients attain good blood levels of CoQ10 on 100mg per day while others require two or three times this amount to attain the same blood level. All CoQ10 available today in the United States is manufactured in Japan and is distributed by a number of companies who place the CoQ10 either in pressed tablets, powder-filled capsules, or oil-based gelcaps. CoQ10 is fat-soluble and absorption is significantly improved when it is chewed with a fat-containing food. However, there is a new form of CoQ10 that will a greater response at a lower dose (see below).
There is no information on the use of CoQ10 for prevention of illness. This is an extremely important question which, to date, has not been answered.
The largest Japanese producer of CoQ10 has patented a novel form of coenzyme Q10 that increases human blood levels up to 8-times more efficiently than expensive CoQ10 products offered by commercial companies.
Coenzyme Q10 exists in both ubiquinol and ubiquinone forms, but they have very different roles to play in the body. For the first time, a stabilized ubiquinol form of CoQ10 is available in capsule form. When compared to conventional (ubiquinone) CoQ10 supplements, the benefits of ubiquinol are enormously superior.
For example, a recent peer-reviewed study measured the absorption in humans supplementing with 150 mg and 300 mg of this new ubiquinol form of coenzyme Q10. Far lower doses of ubiquinol produce about the same blood (plasma) levels compared with much higher doses of ubiquinone. In this study it takes 8-times more ubiquinone to increase CoQ10 blood levels to what can be achieved with much lower doses of ubiquinol.
What may also make this novel form of CoQ10 so much more effective than CoQ10 supplements on the market today is its ability to remain biologically active in the body much longer. In a study on aged rats, blood concentrations of this new ubiquinol CoQ10 was 3.75-fold greater after eight hours compared to the same amount of conventional coenzyme Q10. [Yan J, Fujii K, et al. Exp Gerontol. 2006 Feb;41(2):130-40]
CoQ10 (Ubiquin-one/ol) can help with the following
Research has raised the possibility that people with Parkinson’s might have problems with structures called mitochondria, a spherical or elongated organelle in the cytoplasm of nearly all eukaryotic cells, containing genetic material and many enzymes important for cell metabolism, including those responsible for the conversion of food to usable energy. The researchers who performed this study found that Parkinson’s patients have reduced levels of coenzyme Q10 in their mitochondria. This led the researchers to investigate whether the antioxidant would be useful in treating the disease.
The study involved 80 people who had been diagnosed with Parkinson’s but had not yet received treatment. The participants were randomly assigned to take a daily dose of 300mg, 600mg or 1,200mg of coenzyme Q10 or an inactive pill called a placebo. Patients were evaluated at the start of the study and after one, four, eight, 12 and 16 months.
The progression of Parkinson’s disease was significantly slower in people taking the highest dose of coenzyme Q10. These patients experienced a slower decline in all areas measured by the researchers, including mental and motor skills, but the greatest effect was in the activities of daily living. Compared to placebo, the lower doses of the drug also seemed to slow Parkinson’s, but the differences were not statistically significant. [Archives of Neurology Oct 2002; 59: pp.1523,1541-1550] No currently used drugs slow the progression of Parkinson’s, but act by controlling the symptoms. This places CoQ10 in a unique position, as it appears to slow progression.
CoQ10 is known to be highly concentrated in heart muscle cells due to the high energy requirements of this cell type. The great bulk of clinical work with CoQ10 has focused on heart disease. Specifically, congestive heart failure (from a wide variety of causes) has been strongly correlated with significantly low blood and tissue levels of CoQ10 [Proc. Natl. Acad. Sci., U.S.A., vol. 82(3), pp. 901-904].
The severity of heart failure correlates with the severity of CoQ10 deficiency [Drugs Exptl. Clin. Res. X(7) pp.497-502]. This CoQ10 deficiency may well be a primary causative factor in some types of heart muscle dysfunction while in others it may be a secondary phenomenon. Whether primary, secondary or both, this deficiency of CoQ10 appears to be a major treatable factor in the otherwise inexorable progression of heart failure.
The efficacy and safety of CoQ10 in the treatment of congestive heart failure, whether related to primary cardiomyopathies or secondary forms of heart failure, appears to be well-established.
Pioneering trials of CoQ10 in cases of heart failure involved primarily patients with dilated weak heart muscle of unknown cause (idiopathic dilated cardiomyopathy). CoQ10 was added to standard treatments for heart failure such as fluid pills (diuretics), digitalis preparations, and ACE inhibitors. Several trials involved the comparison between supplemental CoQ10 and placebo on heart function as measured by echocardiography. CoQ10 was given orally in divided doses as a dry tablet chewed with a fat-containing food or an oil-based gel cap swallowed at mealtime.
Heart function, as indicated by the fraction of blood pumped out of the heart with each beat (the ejection fraction), showed a gradual and sustained improvement in tempo with a gradual and sustained improvement in patients’ symptoms of fatigue, shortness of breath, chest pain and palpitations. The degree of improvement was occasionally dramatic with some patients developing a normal heart size and function on CoQ10 alone. Most of these dramatic cases were patients who began CoQ10 shortly after the onset of congestive heart failure. Patients with more established disease frequently showed clear improvement but not a return to normal heart size and function.
A few studies, however, have found no benefit from CoQ10 supplementation in treating people with cardiomyopathy. Despite a partial lack of consistency in the outcomes of published research, most holistic doctors recommend 100-150mg per day taken with meals.
Coenzyme Q10 has also been shown to improve cardiac function in people with hypertrophic cardiomyopathy – a less common form of cardiomyopathy. [Am Heart J 1996;132(Pt 1): pp.61-70]
CoQ10 deficiency is common in individuals with heart disease. Heart tissue biopsies in patients with various heart diseases show a CoQ10 deficiency in 50 to 75% of cases. In one study, patients with stable angina pectoris were treated with CoQ10 at 150 mg per day for four weeks. Compared to placebo, CoQ10 reduced the frequency of anginal attacks by 53%. In addition, there was a significant increase in treadmill exercise tolerance. The results of this study and others suggest that CoQ10 is a safe and effective treatment for angina pectoris.
Eighty-three hypertensive patients were treated with either coenzyme Q10 (60mg bid with 150IU of vitamin E) or placebo with vitamin E. The coQ10 treated group experienced an average reduction in systolic blood pressure of 17.8mm without any significant side effects. [S Med J, November 2001;94(l]): pp.1112-1117]
CoQ10 enhances the pumping action of the heart, output of blood, speed of heart muscle contraction and general cardiac efficiency. Dosage: 60-120mg per day.
Research has shown that orally administered CoQl0 can improve functioning of myocardial tissue, strengthening the heart’s contractions and making it beat more strongly (positive inotropic effect) and more regularly (anti-arrhythmia effect). CoQ10 also acts as an antioxidant to control free radicals produced during cardiac interventions (including angioplasty, thrombolysis, and surgery).
If you are going to have heart or gum surgery, consider adding CoQ10 (100mg BID) before and after surgery.
In a randomized, double-blind, placebo-controlled trial, researchers found that CoQ10 treatment decreased progression and reversed renal dysfunction in a majority of patients with end-stage disease, many of whom were able to discontinue dialysis over the course of the 12-week trial.
Dr. Singh and his colleagues documented significantly lower levels of serum creatinine and blood urea nitrogen in the CoQ10 treated patients, with increases in creatinine clearance and urine output regardless of patient dialysis or baseline status. More significantly, only half the number of CoQ10 patients required dialysis at the end of the study when compared to subjects receiving placebo.
The researchers also reported considerable increases in the antioxidant vitamins E and C and beta-carotene in treated subjects, while plasma levels of oxidative stress such as thiobarbituric acid reactive substances, diene conjugates, and malondialdehyde all fell dramatically.
Although one in five patients did not respond, the researchers concluded that CoQ10 supplementation improves renal function in end-stage patients regardless of dialysis status, and can delay or avert the need for dialysis. They suggested that higher doses than those used in their study (180mg per day) might result in even greater improvement and response in others. [J Nutr Environ Med. 2003;13(1): pp.13-22]
A researcher at the University of Rome in Italy, reported that CoQ10 may improve retinal function in patients with age-related macular degeneration by improving the performance of mitochondria in the retinal pigment epithelium.
Dr. Feher and associates treated 14 patients diagnosed with early age-related macular degeneration using a preparation that included CoQ10, acetyl-L-carnitine, polyunsaturated fatty acids, and vitamin E. A matched control group received vitamin E alone. A number of tests were then performed at 3, 6, 9, 12, and 24 months.
In patients receiving the CoQ10 mixture, all functions were slightly improved after three months and remained level throughout the two-year study period, while degeneration and visual function among participants in the control group continued to slowly decline. [Ophthalmol. 2003 Sept- Oct:217(5):351-7]
Three months of CoQ10 at 100mg bid reduced blood pressure and glycated HbA1c in a well-controlled study of 74 patients with uncomplicated Type 2 diabetes and lipid abnormalities. [Eur J Clin Nutr 2002;56(11): pp.1137-42]
In one double-blind trial, either 120mg of CoQ10 or placebo was given to people who had recently survived a heart attack. After 28 days, the CoQ10 group had experienced significantly fewer repeat heart attacks, fewer deaths from heart disease, and less chest pain than the placebo group.[Cardiovasc Drugs Ther 1998;12: pp.347–53]
In another double-blind study of people suffering a heart attack, supplementation with 60 mg of coenzyme Q10 twice a day for one year significantly reduced the incidence of recurrent cardiac events (fatal or non-fatal heart attack). [Mol Cell Biochem 2003;246: pp.75–82] Treatment was begun within 72 hours of the onset of the heart attack.
CoQ10 used with selenium (see below) has also been reported to increase the rate of heart attack survival. [Mol Aspects Med 1994;15 Suppl:s143–7]
There are sound theoretical reasons to add 400 mg of highly absorbable CoQ10 to any anti-cancer protocol. This dosage has initiated complete tumor regression in breast cancer patients. As the pancreas has a high concentration of CoQ10, it may be that restoring CoQ10 levels improves pancreatic function, which can help prevent and treat cancer, according to the John Beard theory of cancer.
Studies suggest that coenzyme Q10 levels are lower in women who have had a recent miscarriage. Similar to methionine and homocysteine normalization, the production of coenzyme Q10 in the body also depends on folic acid, vitamin B12, and betaine.
|May do some good|
|Likely to help|
A heat stable molecule that must be associated with another enzyme for the enzyme to perform its function in the body. It is necessary in the utilization of vitamins and minerals.
A chemical compound that slows or prevents oxygen from reacting with other compounds. Some antioxidants have been shown to have cancer-protecting potential because they neutralize free radicals. Examples include vitamins C and E, alpha lipoic acid, beta carotene, the minerals selenium, zinc, and germanium, superoxide dismutase (SOD), coenzyme Q10, catalase, and some amino acids, like cystiene. Other nutrient sources include grape seed extract, curcumin, gingko, green tea, olive leaf, policosanol and pycnogenol.
454 grams, or about half a kilogram.
(mg): 1/1,000 of a gram by weight.
Usually Chronic illness: Illness extending over a long period of time.
Essential mineral that is essential to nutrition. Nutritionists prefer to call minerals either minerals or trace minerals depending on the amount needed by the body, while analytical chemists prefer to call minerals, trace elements.
A waxy, fat-like substance manufactured in the liver and found in all tissues, it facilitates the transport and absorption of fatty acids. In foods, only animal products contain cholesterol. An excess of cholesterol in the bloodstream can contribute to the development of atherosclerosis.
An illness or symptom of sudden onset, which generally has a short duration.
Pertaining to the relaxation phase of the heartbeat, or period when the heart muscle is resting and filling with blood. When used in blood pressure readings (for example 120/80), it refers to the second/lower number.
Pertaining to the heart, also, pertaining to the stomach area adjacent to the esophagus.
High blood pressure. Hypertension increases the risk of heart attack, stroke, and kidney failure because it adds to the workload of the heart, causing it to enlarge and, over time, to weaken; in addition, it may damage the walls of the arteries.