|CoEnzyme Q10 for Healthy Hearts|
|Written by John Williamson Cameron|
|Friday, 13 March 2009 14:02|
Coenzyme Q10 is a fat-soluble vitamin-like substance present in every cell of the body, which serves as a coenzyme for several of the key enzymatic steps in synthesis of ATP on which production of energy within all cells depends. In its reduced form, called ubiquinol, Coenzyme Q10 is a potent anti-oxidant that protects cells from damage by free radicals. It also regenerates other anti-oxidants, including vitamins C and E.
CoQ10 was first isolated from beef heart mitochondria in 1957, and it was first synthesized in 1958. In 1972, Gian Paolo Littaru of Italy along with Professor Karl Folkers of the US documented a deficiency of CoQ10 in human heart disease. By the mid 1970s, the Japanese had perfected the industrial technology to produce pure CoQ10 in quantities sufficient for larger studies.
In the early 1980s, scientists were able to conduct a number of clinical trials due to the availability of CoQ10 in large quantities from Japan and from the newly acquired capacity to measure CoQ10 in blood and tissue. Professor Karl Folkers received the Priestly Medal in 1986 and the National Medal of Science from President Bush in 1990 for his work with CoQ10 and other vitamins. Internationally, a dozen placebo controlled studies on treatment of heart disease with CoQ10 have confirmed the effectiveness of CoQ10 in improving heart muscle function while producing no adverse side effects or drug interactions.
Because CoQ10 is a natural substance, it can not be patented, so patent-protected profits have not been available to educate physicians and the public about the proven benefits of CoQ10 for the treatment of heart failure. The lack of patent-protected profits has also prevented the automation of the complex, seventeen-step process required for measurement of CoQ10 blood levels by gas chromatography. Even today, only a half dozen labs in the United States are capable of testing CoQ10 levels. CoQ10 has shown great promise in preliminary studies in treatment of many other conditions, but lack of patent-protected profits and lack of an automated economical system for testing CoQ10 have severely limited large-scale clinical studies.1
CoQ10 is present in small amounts in a wide variety of foods but the dominant source of CoQ10 in humans is biosynthesis. CoQ10 required by blood cells is synthesized in the liver, while the majority of CoQ10 synthesis occurs in cells throughout the body.
The biosynthesis of CoQ10 is a complex multi-step process that requires at least seven vitamins (B2, B3, B5, B6, B12, C and folic acid) and several trace elements, and is, by its nature, highly vulnerable. Sub-optimal nutrient intake impairing CoQ10 synthesis is almost universal, and deficiency of any of the vitamins or trace elements required for CoQ10 synthesis can cause deficiency of CoQ10. Decreased absorption of nutrients necessary for synthesis of CoQ10 can be caused by aging,2 digestive problems such as irritable bowel syndrome,3 liver diseases,4 and many common prescription drugs5 including oral contraceptives6 and HRT.7
CoQ10 synthesis can also be impaired by the widely prescribed HMG-CoA reductase inhibitors (statins) which block the synthesis of melovonic acid and thereby block synthesis of cholesterol, CoQ10 and other compounds, such as squalene and isoprene, all of which are important to health.
Increased utilization of CoQ10 by the body is the cause of low blood CoQ10 levels seen in many conditions, including excessive exertion,1 hyperthyroidism,8 aortic valve stenosis,9 hypertrophic cardiomyoathy,10 diabetes,11 rheumatoid arthritis,12 lupus,13 HIV,1 asthma,14 certain cancers, 15 hyperlipidemia,16 and atherosclerosis.17
Researchers now consider CoQ10 deficiency to be a significant cause of heart failure and coronary artery disease. CoQ10 deficiency also is thought to contribute to cancer, infertility in men18 and migraine headache.19
Overview of Heart Failure
Much of the media coverage and advertising on the subject of heart disease is misleading, unbalanced or erroneous. The term â€ścardiovascular diseaseâ€ť is often carelessly used in public discourse as though it were synonymous with â€śheart disease,â€ť thereby implying that all heart disease is due to blockage of coronary arteries. As a result of widespread misinformation, many incorrectly believe that all heart failure is the result of coronary artery disease.
The primary cause of impaired systolic function is heart muscle damage caused by reduced blood flow due to coronary artery disease. While the damage can result from chronic reduced blood flow through narrowed arteries, it is most often due to plaque rupture, which causes a sudden complete artery blockage that precipitates a heart attack. The common measure of systolic function is â€śejection fraction,â€ť the percent of ventricle volume discharged with each heart contraction. Systolic function is considered impaired when the ejection fraction is less than 45 percent compared to the normal range of 55 to 70 percent and the borderline range of 45 to 54 percent. Clinical trials of heart disease treatments have focused for decades on young men with â€śimpairedâ€ť systolic function. It is now recognized that over 90 percent of cardiac deaths occur in men and women over 65 years of age, and more than half of cardiac deaths occur in those with â€śnormalâ€ť systolic function.20
Past focus on impaired systolic function occurred largely because the importance of the filling phase of the heart cycle, the diastolic phase, had been little studied and was poorly understood. The term â€śdiastolic heart failure,â€ť meaning heart failure resulting from impaired diastolic function in those with â€śnormalâ€ť ejection fraction, first appeared in clinical studies about ten years ago, and one medical texts described diastolic heart failure as a â€śnewâ€ť type of heart failure.21 Diastolic dysfunction leading to diastolic heart failure is due primarily to deficiency of CoQ10 which causes energy starvation of the heart.
Whenever systolic function is impaired, diastolic dysfunction is also present, and the degree of diastolic dysfunction has been found to more accurately predict the prognosis of systolic heart failure than ejection fraction, the common measure of systolic impairment. While coronary artery disease is the primary cause of heart failure with impaired systolic function, the conditions that lead to coronary artery disease also increase CoQ10 utilization and can result in CoQ10 deficiency and diastolic heart failure.
The mortality rate of heart failure cases with impaired systolic function is almost double the mortality rate of diastolic heart failure, but the total number of deaths due to the two conditions is approximately equal due to the greater number of those with diastolic heart failure.20
Causes Of Coronary Artery Disease (CAD)
There are many factors that contribute to development of atherosclerosis, but the primary cause is the profound changes that have taken place in the American diet during the past century, particularly:
The typical American diet results in increased production of triglycerides (TG), decreased levels of HDL-cholesterol, and a preponderance of small, dense LDL-cholesterol particles, a condition referred to as the atherogenic lipid triad. The increase in the atherogenic potential of LDL arises from the increase in the number of small, dense LDL particles, not from the cholesterol content per se. Small dense LDL particles more easily penetrate the arterial wall, initiating atherosclerotic injury, which leads to the development of inflammation and plaque.23
The development of highly atherogenic, small dense LDL particles is thought to be due to high insulin levels and excess triglycerides that result from excessive carbohydrate and caloric intake and from an imbalance of essential fatty acids.24,25 Researchers have noted a high degree of correlation between the TG/HDL ratio, insulin intolerance, particle size and the presence of coronary artery disease. Because TG and HDL are commonly measured, the ratio TG/HDL is considered proxy for LDL particle size and a good indicator of the presence of coronary artery disease (CAD) and risk of adverse coronary events.26
High insulin levels cause insulin intolerance and diabetes, and together these greatly increase the risk of coronary artery disease. In one study, 58 percent of CAD patients were found to be insulin resistant, including 22 percent with diabetes. Diabetes and insulin intolerance greatly increase the risk of cardiac death.27
The increased oxidative stress resulting from coronary artery disease increases utilization of ubiquinol, the reduced form of CoQ10, resulting in low levels of both total CoQ10 and ubiquinol. Levels of ubiquinol in those with CAD have been found to be inversely proportional to triglyceride levels.15 Diabetes causes severe depression of CoQ10 levels, and because development of CAD usually occurs slowly, diastolic heart failure is common in diabetic patients.
Other factors that contribute to atherosclerosis are smoking, inactivity and stress. The stress factor can result from an imbalance of essential fatty acids due to excess production of â€śbadâ€ť eicosanoids (hormones) that promote the â€śfight or flight responseâ€ť and which cause an exaggerated response to normal daily stress. Exaggerated stress response can result in many physiological changes that contribute to coronary artery disease, including increased adrenaline production leading to constriction of blood vessels, increased blood clotting factors, and stimulation of smooth muscle cell production.22
In addition, trans fatty acids and nutrient deficiencies, particularly deficiency in vitamin A, make it difficult for the body to produce hormones needed for dealing with stress.
Adoption of a nutrient-dense, low-carbohydrate diet with a balance of essential fatty acids can profoundly shift the physiological state to one that is anti-atherogenic, with normalized insulin and lipid levels. Such improvements in diet will not significantly reverse established diabetes or coronary artery disease, but will reduce their rate of progression. It is not unusual for those who adopt a healthy low-carbohydrate diet to experience a reduction of the TG/HDL ratio by 50 to 75 percent, indicating a dramatic decrease in insulin resistance, inflammation, and levels of small LDL particles, and further indicating reduced risk of diabetes, coronary artery disease and adverse cardiac events.28
The beneficial effects of a nutrient-dense, low-carbohydrate diet with balanced essential fatty acids is seen in the low rates of diabetes and heart disease in those who follow this type of diet, such as those in some fishing villages in Japan and Intuit natives.29,30 Autopsies have found significantly lower levels of atherosclerosis in such populations compared to neighboring populations on diets containing modern processed foods.
Cholesterol performs many important functions in the body and cholesterol levels increase with age in response to increased need. Research indicates that those with cholesterol above 240 have better brain function and live longer than those with cholesterol below the prescribed â€śhealthyâ€ť level of 200. The increased incidence of cancer observed in statin users may be due in part to reduced cholesterol levels, which result in reduced synthesis of vitamin D from sunlight.31,32 Saturated fat, which has been erroneously demonized as a cause of high cholesterol levels, does not stimulate insulin production and thus cannot cause increased cholesterol levels.22
The typical pro-atherogenic American diet has been made far worse by ill-advised government policies, which encourage increased consumption of carbohydrates and omega-6 polyunsaturated oils and discourage consumption of healthy saturated fat and protein. As a result, the majority of older people have some degree of atherosclerosis and many have coronary artery disease.
CoQ10 Deficiency and Diastolic Dysfunction
The filling phase of the heart requires more energy than the contraction phase, and is therefore more sensitive to CoQ10 deficiency. Energy starvation of the heart due to CoQ10 deficiency causes stiffening of the heart walls in the left ventricle and results in impaired filling of the heart, or diastolic dysfunction. Fatigue or lack of energy is a common symptom of diastolic dysfunction. The stiffened heart walls increase energy requirements of the heart thereby increasing CoQ10 utilization and further depleting CoQ10 reserves. A vicious cycle ensues. As diastolic dysfunction worsens, blood pressure and heart rate increase, the heart walls thicken, and pulmonary hypertension often develops. When diastolic dysfunction is sufficient to produce pulmonary congestion (that is, a damming up of blood into the lungs causing shortness of breath), congestive heart failure is said to be present. Estimates indicate that 15 percent of those under age 50 and 50 percent of those over age 70 have diastolic dysfunction, and more than half of those presenting with acute pulmonary congestion have diastolic heart failure.21
The finding that diastolic dysfunction is caused by CoQ10 deficiency is not reflected in the majority of medical references. Mainstream medicine insists that diastolic dysfunction is due to many causes, including chronic hypertension, hypertrophic cardiomyopathy, aortic stenosis, coronary artery disease, diabetes and aging. All of the conditions considered â€ścausesâ€ť of diastolic dysfunction increase utilization of CoQ10 and cause CoQ10 deficiency, and all can be improved with CoQ10 supplementation.
Systolic heart dysfunction caused by coronary artery disease and diastolic dysfunction due to CoQ10 deficiency are both common in the older population. In a recent study of men and women over age 65, about 5 percent were diagnosed with heart failure. Of those with heart failure, 63 percent had normal systolic function or diastolic heart failure, while only 15 percent had borderline systolic function and 22 percent had impaired systolic function. Men outnumbered women by three to one in those with impaired systolic function, while women slightly outnumbered men in those with normal systolic function.20
Treatment Of Heart Disease With CoQ10
The normal range of CoQ10 in the blood is 0.6 to 2.0 mcg/ml. CoQ10 levels in the low normal range are an indication of conditions that increase utilization or decrease synthesis of CoQ10. Since CoQ10 deficiency is widespread, average levels of CoQ10 are actually considered to be less than optimum. In many of the studies of heart disease treatment with CoQ10, patients were given a fixed amount of CoQ10 on the order of 100 mg/day. More recently it has become the practice of some physicians to adjust CoQ10 dosage toÂ achieve a minimum blood level of 2.0 mcg/ml. This usually requires dosages of from 200 to 500 mg per day. CoQ10 supplements are divided into doses of no more than 150 mg each, usually taken with meals for most efficient absorption.33
The symptoms of fatigue and activity impairment, myalgia, and cardiac arrhythmia frequently precede by years the development of congestive heart failure and are the result of diastolic dysfunction caused by CoQ10 deficiency. Supplemental CoQ10 is unique in its ability to improve diastolic dysfunction and bring about a normalization of blood pressure, heart rate and ventricular hypertrophy that are symptoms of diastolic dysfunction. Accordingly, conditions that cause diastolic dysfunction are addressed first below.34
An overactive thyroid causes a high rate of metabolism or energy use, which results in increased utilization of CoQ10 and can result in CoQ10 levels that are among the lowest detected in human diseases. Hyperthyroidism will lead to heart failure if not corrected. CoQ10 supplementation can normalize cardiac function, but correction of thyroid production usually will normalize metabolism, CoQ10 levels and diastolic function.8
Statin Drug Use
The depletion of the essential nutrient CoQ10 by the popular cholesterol-lowering drugs, HMG CoA reductase inhibitors (statins) is dose related. A clinical trial in which subjects took 80 mg per day of atorvastatin (Lipitor) resulted in a reduction of CoQ10 by 50 percent within 30 days. It was concluded that statin-induced CoQ10 deficiency was the probable cause of the most commonly reported side effects of statinsâ€”muscle pain, exercise intolerance, and fatigue.35
Another clinical trial found that CoQ10 deficiency caused by atorvastatin therapy worsened left ventricular diastolic function in most patients. CoQ10 supplementation in patients with worsening diastolic function resulted in improved diastolic function.36
In a recent clinical study, patients who had been on statins for an average of 28 months were evaluated for adverse statin effects, including muscle pain, fatigue, shortness of breath, memory loss and peripheral neuropathy. All patients discontinued statins due to side effects and began supplemental CoQ10 at an average of 240 mg per day. After a period of 22 months, patients experienced a decrease in fatigue from 84 to 16 percent, muscle pain from 64 to 6 percent, shortness of breath from 58 to 12 percent, memory loss from 8 to 4 percent and peripheral neuropathy from 10 to 2 percent. Heart function improved or remained stable in the majority of patients and there were no adverse consequences from statin discontinuation. It was concluded that statin-related side effects are far more common than previously recognized and are reversible with a combination of statin discontinuation and supplemental CoQ10.37
Cholesterol performs many valuable functions in the body that can be impaired by reduction of cholesterol levels with statins. For example, cells in the brain produce cholesterol because the cholesterol molecule is too large to pass the brain-blood barrier.38 Statins can pass the blood-brain barrier and reduce brain levels of cholesterol. A recent clinical study found that those taking statins had minor impaired mental function compared to controls not on statins.39
Secondary hypertension, or hypertension from known causes, such as renal artery stenosis and hardened arteries, is the cause of less than 10 percent of hypertension, while hypertension from unknown causes, or â€śessential hypertension,â€ť comprises the remaining 90 percent. Secondary hypertension increases the energy requirements of the heart, thereby increasing CoQ10 utilization and resulting diastolic dysfunction. Standard dogma in cardiology has long held that diastolic dysfunction is caused by both secondary and essential hypertension, but evidence from treatment of hypertension with CoQ10 suggests that diastolic dysfunction is the cause, not the result, of hypertension from unknown causes.
The vast majority of patients with hypertension have diastolic dysfunction regardless of whether the blood pressure is treated or untreated, or controlled or uncontrolled. Supplemental CoQ10 is unique in its ability to improve diastolic dysfunction, and as diastolic function improves, blood pressure in patients taking anti-hypertensive drugs drifts down so that more than one fourth of patients attain normal blood pressure and require no more anti-hypertensive drugs. The remaining patients require substantially less anti-hypertensive drug therapy.
Patients with diastolic dysfunction have impairment of the filling phase of the cardiac cycle, which limits the ability to increase cardiac output, and cardiac output can only be increased by increasing heart rate and blood pressure. It has been postulated that the normalization of blood pressure which occurs as a result of CoQ10 supplementation is the result of the normalization of diastolic functionâ€”the ability of the heart to expand and fill moreâ€”and thus increase cardiac output.40,41
There have been numerous studies using CoQ10 for treatment of hypertension in patients not on anti-hypertensive drugs. In eight studies, the mean decrease in systolic blood pressure was 16 mmHg and in diastolic pressure, 10 mmHg.42
Other beneficial effects of CoQ10 include reduction of endothelial dysfunction, peripheral resistance and blood viscosity, thereby reducing blood pressure and improving circulation and delivery of oxygen to tissues. CoQ10 also normalizes blood pressure by reducing oxidative damage to cells through the anti-oxidant action of the reduced form of CoQ10, ubiquinol.
Hypertrophic cardiomyopathy (HCM) is a genetic abnormality manifested by severe thickening of the left ventricle, a condition that increases energy requirements of the heart and increased utilization of CoQ10. The resulting CoQ10 deficiency can cause significant diastolic dysfunction with disabling cardiac symptoms and increased risk of sudden death at any age. In a clinical trial on HCM treatment with CoQ10 supplementation, ventricular wall thicknesses were reduced by 25 percent to near normal levels and symptoms of diastolic dysfunction, including fatigue and shortness of breath, were greatly reduced.10
Heart Dysfunction In The Elderly
Current medical texts often list aging as one of the many causes of diastolic dysfunction. Diastolic dysfunction is common in the elderly due to increased oxidative stress. Diastolic dysfunction shows clear improvement with use of CoQ10, even in those of advanced age. Elderly patients, average age 84 years, experienced significant improvement in diastolic dysfunction, exercise tolerance and quality of life when treated with an average CoQ10 dose of 220 mg per day. These findings refute the common assertion that a stiff and non-compliant heart is a normal and irreversible aspect of the aging process.53
Congestive Heart Failure
The main clinical problems in patients with congestive heart failure are frequent hospitalizations due to the high incidence of life-threatening arrhythmias, pulmonary edema and other serious complications.
In a trial that studied the influence of longterm CoQ10 treatment on patients with chronic heart failure receiving conventional treatment, patients were randomized to receive a placebo or 2 mg per kilogram of body weight per day CoQ10. Compared to those in the placebo group, patients receiving CoQ10 in addition to conventional therapy had 38 percent fewer hospitalizations, 61 percent fewer episodes of pulmonary edema, and 51 percent fewer episodes of cardiac asthma. The results showed that addition of CoQ10 to conventional therapy significantly reduced hospitalizations for worsening heart failure and the incidence of serious complications.54
CoQ10 for Heart Attack Patients
In a one-year, double-blind controlled trial of patients who had suffered a recent heart attack, the effects of 120 mg per day of CoQ10 were compared with effects of a placebo. The two groups were similar with respect to the extent and history of their heart disease, and both groups were receiving â€śoptimal lipid therapyâ€ť with about half the patients in each group taking 10 mg per day of Lovastatin. Compared to those in the placebo group, patients receiving CoQ10 in addition to conventional therapy had 44 percent fewer episodes of total cardiac events, 44 percent fewer non-fatal infarctions, significantly lower cardiac deaths, 83 percent fewer patients reporting fatigue, and a significant decrease in markers of atherosclerosis.55
CoQ10 for Diabetic Patients
Diastolic dysfunction often in the absence of coronary artery disease is more prevalent in diabetics than in the general population. It has been estimated that approximately 75 percent of those with diabetes will eventually die from some kind of heart problem, compared to 25 percent of the general population. CoQ10 supplements of 200 mg per day have been found to improve blood pressure, glycemic control and endothelial (circulatory) function in patients with type-2 diabetes. Control of endothelial function is of great importance because of the prevalence of circulatory problems in diabetics.51,56
CoQ10, a substance found in all cells of the body, is essential for using the energy you breath to make the cellular energy source ATP. CoQ10 deficiency results in impaired heart function, particularly dysfunction of the filling phase of the heart cycle. Diastolic dysfunction is present in all heart failure, whether the heart failure is due primarily to CoQ10 deficiency, coronary artery disease, or some other cause.
Synthesis of CoQ10 declines with age due to decreased absorption of the nutrients needed for CoQ10 synthesis and the increased utilization of CoQ10 from a natural increase in oxidative stress. CoQ10 synthesis can be further depressed by a number of congenital conditions such as type-1 diabetes and some autoimmune diseases, and by self-inflicted physiological conditions such as insulin intolerance, type-2 diabetes and coronary artery disease, all of which are caused by high insulin levels that result from a diet with excess carbohydrates and omega-6 fatty acids and inadequate omega-3. Thus, the misguided, â€śpolitically correctâ€ť dietary recommendations are a major contributor to coronary artery disease so prevalent in the western world. Depletion of CoQ10 levels can be exacerbated by many drugs that are widely prescribed to the elderly, particularly the cholesterol-lowering statins, which directly inhibit CoQ10 synthesis.
CoQ10 is naturally present in the body so CoQ10 supplementation causes virtually no side effects. CoQ10 supplementation can prevent development of diastolic dysfunction and the accompanying symptoms of hypertension and fatigue and, when used in conjunction with proper diet, can reduce the risk of coronary artery disease and diabetes. CoQ10 supplementation is also thought to reduce the risk of many other diseases and conditions, including cancer, immune diseases, migraine headache, male infertility and the increased oxidative stress that occurs with aging.
Of course, the first line of defence should be a nutrient-dense traditional diet, including liver and raw animal foods, which supply the vitamins and minerals needed for synthesis of CoQ10. These foods are just as important for protecting seniors as they are for building strong bodies in the young.
Coenzyme Q10 And Cancer
Abnormally low plasma CoQ10 levels have been found in patients with melanoma and cancer of the breast, lung and pancreas.A Early studies have hinted that CoQ10 may be effective in treating some cancers. In one study, six of 32 patients who took 90 mg per day of CoQ10 showed partial tumor reduction. One of the six then began taking 390 mg per day, and within two months there was no mammographic evidence of the tumor.B An additional three patients undergoing conventional treatment took 390 mg of CoQ10 over three to five years. The results: in patient one, liver metastases disappeared; in patient two, the tumor in the pleural cavity disappeared; in patient three, there was no sign of cancer in the tumor bed nor of metastases.C
Abnormally low concentrations of CoQ10 were found to be a strong predictor of metastasis in patients with melanoma. Patients with melanoma and matched controls were followed over seven and one-half years. The average CoQ10 levels of patients at baseline was 0.50 mcg/ml compared to 1.27 mcg/ml in controls. It was found than 33 percent of melanoma patients developed metastases during the follow-up period. The patients who developed metastases during follow-up had baseline CoQ10 levels of 0.34 mcg/ml compared with a level of 0.57 mcg/ml in patients who did not develop metastases. Patients with low baseline CoQ10 levels had an approximate eight-fold risk of metastatic disease compared with patients with high levels. It was concluded the baseline CoQ10 levels are a powerful and independent prognostic factor that can be used to estimate the risk for melanoma progression.A The foregoing study suggests the probability that CoQ10 supplementation may greatly reduce the risk of metastases in melanoma patients.
In cancer, abnormal cell growth occurs because cells have lost their ability to kill themselves, a process called apoptosis. A recent study suggests that supplementing with CoQ10 can restore the ability of the cancer cell to kill itself. Gene analysis has found that the bci-2 genes regulate cell division and programmed cell death. Cells normally divide and unneeded or sick cells are eliminated, but in cancer there is a decrease in cell death and the cells keep dividing. Both CoQ10 and bci-2 are present in normal and malignant cells, but in cancer patients there is an over-expression of bci-2 and a deficiency of CoQ10. Under these conditions, the cells canâ€™t self destruct, resulting in cell proliferation. The researchers concluded that CoQ10 supplementation helps restore the ability of cancer cells to kill themselves.D
Another study found that CoQ10 supplementation reduces the side effects of chemotherapy.E
While no large long-term studies have yet been carried out on use of CoQ10 to treat cancer, it would seem prudent and beneficial for cancer patients to take CoQ10 supplements based on information available to date.
References for this sidebar
Coenzyme Q10 and Food
Research indicates that the body requires replacement of about 500 mg per day of CoQ10.a The average CoQ10 content of the western diet is about 5 mg per day, so for most people, food contributes only about 1 percent of daily CoQ10 requirementsâ€”the balance comes from endogenous synthesis. The highest level of CoQ10 is found in heart meat, and significant amounts are found in cold water fish, beef, pork, chicken and nuts. About 10 percent of daily CoQ10 requirements can be obtained by eating 12 ounces of beef or pork heart, two pounds of sardines or mackerel, three pounds of beef or pork, or four pounds of peanuts. Milk, eggs, and most grains and vegetables contain small amounts of CoQ10.b
Synthesis of CoQ10 indispensably requires vitamins B2, B6, B12, C, folic acid, niacin and pantothenic acid along with several trace elements, including selenium, which protects CoQ10 from oxidation.c,d Deficiencies in any of these nutrients can result in reduced synthesis of CoQ10 and cause many other adverse effects as well. The vitamin and mineral content of foods is therefore of greater importance for maintaining CoQ10 levels than their CoQ10 content. Most of the foods that contain significant amounts of CoQ10 are also rich in many of the nutrients required for CoQ10 synthesis.
Synthesis of CoQ10 declines with age.e A study of plasma levels of CoQ10 and vitamin B6 in the elderly found that indicators of vitamin B6 activity declined with age, and that CoQ10 levels were directly related to levels of B6 activity,f indicating that reduced CoQ10 levels result from low levels of vitamin B6. Vitamin B12 is also required for CoQ10 synthesis, and absorption of B12 declines with age. Advanced age therefore increases the importance of adequate intake of the nutrients required for synthesis of CoQ10, including nutrient-dense foods like liver and raw animal foods as sources of vitamin B6.
Many inflammatory conditions that result in oxidative stress and reduced CoQ10 levels, such as insulin intolerance, diabetes and atherosclerosis, can be prevented or improved by proper diet. A balanced, healthy diet is necessary to provide the nutrients needed for optimum CoQ10 synthesis and for maintenance of a physiological state that minimizes the oxidative stress that that leads to decreased CoQ10 levels.
References for this sidebar
CoQ10, Vitamin E, and Coronary Artery Disease
There are a number of forms of vitamin E that occur in foods, but alpha-tocopherol is the only form that is retained by the body in significant amounts and is therefore considered the form of vitamin E most important to health.43 CoQ10 supplementation regenerates the oxidized form of alpha-tocopherol to the active reduced form. It has been hypothesized that CoQ10 is essential for the beneficial function of alpha-tocopherol.44
For a long time vitamin E was assumed to act by decreasing the oxidation of small dense LDL particles, which play a key role in atherosclerosis initiation. However, it has been found that at the cellular level, vitamin E acts by inhibiting many reactions involved in progression of atherosclerosis, including inhibition of smooth muscle cell proliferation, platelet aggregation, monocyte adhesion, oxLDL uptake, cykotine production and superoxide production. Oxidation impairs the beneficial functions of alpha-tocopherol, so regeneration of alpha-tocopherol by CoQ10 is important for preventing coronary artery disease.45
CoQ10, Omega-3 and Heart Disease
More than 20,000 clinical studies have explored the health benefits of omega-3 fatty acids, a large portion of which related to treatment of heart disease. A study in Italy of over 11,000 heart attack patients found that one gram per day of omega-3 fatty acids significantly reduced the mortality rate in the coming years, a record far better than that experienced by statin drug users, and without the adverse side effects. While the beneficial functions of omega-3 fatty acids are multiple, the researchers concluded that the reduction of mortality resulting in the aforementioned study was the result of a reduction in cardiac arrhythmias. As a result of the study, use of omega-3 supplementation following myocardial infarction has become standard protocol in Europe.46
EPA and DHA, the long-chain omega-3 fatty acids which are most important to heart health, are not present in plant foods but are abundant in cold water fish. EPA can be synthesized by the body from the omega-3 fatty acids found in plant food, but it is questionable whether DHA can be synthesized in adequate amounts, if at all. Synthesis of EPA is impaired by excessive omega-6 and carbohydrate intake and by trans fats. It has been hypothesized that CoQ10 may protect the sensitive DHA double bonds from destruction by oxidation.47
Animal studies illustrate that vitamin B6 and folate metabolism are linked with those of long-chain fatty acids. Furthermore, a human study indicated synergistic effects of folic acid and vitamin B6 together with omega-3 fatty acids on the atherogenic index.48 Omega-3 fatty acids therefore enhance CoQ10 synthesis through enhancement of B vitamin metabolism.
The beneficial functions of alpha-tocopherol in inhibiting development of atherosclerosis are also brought about by supplementation with EPA and DHA. In addition, EPA and DHA supplements have been found to improve endothelial function and insulin resistance, reduce thrombosis, reduce triglycerides and increase HDL-cholesterol.49,50
CoQ10 has been found to improve endothelial function and peripheral resistance, both of which indicate poor circulation when compromised, leading to coronary artery disease. CoQ10 supplementation also reduces triglyceride levels, glucose levels and insulin resistance and increases HDL levels.51,52
Aortic stenosis, the incomplete opening of the aortic valve, increases the work load on the heart, thereby causing CoQ10 deficiency and diastolic dysfunction. A major cause of aortic stenosis is a bicuspid valve, a genetic abnormality in which the aortic valve has two cusps rather than the normal three cusps. Calcification and narrowing of a bicuspid aortic valve often begins in the fourth or fifth decade of life. Aortic stenosis can also occur in a normal valve, usually in the seventh and eighth decade of life, due to normal wear and tear. When symptoms of heart failure occur, valve replacement is the treatment of choice. Over half of valve replacements are in those with a bicuspid valve.
CoQ10 supplementation greatly improves heart function in aortic stenosis. While there have been no published studies on treatment of aortic stenosis with CoQ10, cardiologists in private practice have observed near normalization of heart function in patients with mild to moderate aortic stenosis using CoQ10 treatment.57 The hypothesis that CoQ10 supplements improve diastolic function by increasing ATP synthesis is illustrated by the fact that aoric stenosis patients have imparied ATP synthesis which normalizes after valve replacement.9
In practice, elderly aortic stenosis patients are often denied surgical valve replacement. An analysis of long-term survival of patients over 70 years of age found that only patients with high baseline risk had a significantly better three-year survival than patients denied surgical treatment. In low-risk patients, those denied valve replacement had better a better survival rate than those who had valve replacement.58
Valve replacement in those with high baseline risk usually results in improvement of diastolic function, but often significant diastolic dysfunction remains, as indicated by pulmonary hypertension. Thus, it is reasonable to conclude that those patients who do benefit from valve replacement would also benefit from CoQ10 supplementation following valve replacement.
Laboratory Tests For Plasma CoQ10
Measurement of blood levels of CoQ10 can determine whether or not supplementation is needed, as well as the effectiveness of supplementation in raising CoQ10 levels. Ubiquinol, the reduced form of CoQ10, is a potent anti-oxidant that protects cells from damage by free radicals, and determination of the ratio of ubiquinol to total CoQ10 provides a measure of the risk of coronary artery disease. The ratio of CoQ10 to cholesterol indicates the level of protection of cholesterol against free radical damage. Vitamin E is also important because of the synergism between vitamin E and CoQ10,
At present there are only three labs in the US that provide testing for CoQ10 and three others that researchers use only for research. The most advance lab for CoQ10 testing in the US is the Langsjoen Q10 Laboratory, Inc., located in the Langsjoen Cardiology Clinic in Tyler, Texas. This extremely accurate, high-pressure liquid chromatography laboratory can measure total and reduced CoQ10 levels in both blood and heart muscle. The unit also measures the ratio of CoQ10 to cholesterol and vitamin E levels. The only other such laboratories are located in Italy and Japan.
Individuals can have CoQ10 levels tested at the Langsjoen laboratory. Lab personnel can assist patients in arranging for samples to be drawn locally, preferably on a Monday. The samples must be shipped overnight packed in dry ice to the Langsjoen lab. Samples are tested and the results mailed to the patient. There is a significant degree of variation between individuals in absorption of CoQ10 supplements, particularly among those with significant heart impairment, so determination of supplemented blood levels is important for optimal treatment.
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About the Author
Diastolic Heart Failure
written by syra, Oct 08 2010
Diastolic Heart Failure
written by syra, Oct 08 2010
|Last Updated on Saturday, 08 August 2009 22:14|