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We have compiled a series of informative articles on antioxidants, these reports are linked to the antioxidants we have selected as the most potent and effective available. You may also scroll down this page and read the most important of these studies. These published clinical studies prove conclusively that neutralizing free radicals is the most important measure you can do today to preserve and improve your health, and both extend your lifespan and its quality. Failure to begin an active program of antioxidant supplementation may well lead to both many diseases associated with aging amd a premature death.
FASEB MEETING: Antioxidants May Reduce Harmful Complications Of Diabetes
April 2, 2000
Duke University Medical Center researchers have found that the depletion of body chemicals called antioxidants may increase the risk of complications from the most common form of diabetes.
The scientists recommend that diabetics take antioxidant supplements, such as vitamin C or E, to help stave off or even forestall the hallmark complications of diabetes, including blindness, kidney failure, amputation and even death.
Antioxidants neutralise oxygen free radicals, highly-reactive chemicals that are the potentially-destructive by-products of the body's process of turning food into energy. Normally, the body produces enough antioxidants of its own to keep the reactive oxygen from causing damage.
"We were able to show that patients with poor control of their diabetes who were beginning to show signs of complications had depleted their store of antioxidants," said Duke researcher Dr. Emmanuel Opara. "Further, we found a significant correlation between high blood-sugar levels and depletion of antioxidants.
"It appears that this depletion is a major risk factor for developing complications and that antioxidant supplements could lower this risk."
Opara presented his studies yesterday at Experimental Biology `98, the annual scientific meeting of the Federation of American Societies for Experimental Biology (FASEB).
The researchers studied 50 similar people with Type II diabetes -- also known as non-insulin-dependent or adult-onset diabetes. In this form of the disease, insulin produced in the body is unable to trigger the lowering of high blood sugar. Type II diabetes afflicts about 90 percent of the estimated 10.7 million Americans diagnosed with the disease and the 5.4 million believed to have undiagnosed cases, according to the Centers for Disease Control and Prevention.
Insulin is the hormone that normally regulates the level of sugar (glucose) in the blood and is produced by cells in the pancreas. Insulin is secreted when the level of blood glucose rises -- as after a meal.
All diabetic patients in the study were taking only drugs referred to as sulfonylureas, which increase the sensitivity of receptors to insulin throughout the body. Half the patients exhibited microalbuminuria, the excretion of tiny amounts of protein in the urine that is considered a precursor of kidney disease, while the other half did not. The researchers took blood samples from all 50 patients, as well as a control group of 20 similar people without diabetes and determined levels of antioxidants in their blood.
"We found that the non-diabetics' ability to defend against damage from the oxygen free radicals was almost twice that of those patients exhibiting microalbuminuria," Opara explained. "And while the difference between the two diabetic groups was not as pronounced, the difference was still statistically significant. Also, antioxidant depletion correlated with high blood sugar after meals only in the group with microalbuminuria."
The researchers determined antioxidant levels by a new chemical assay developed at King's College in England that enabled them to measure all known antioxidants in the blood and to obtain a more global picture of the body's total antioxidant capacity, Opara said. Other assays are only specific for individual antioxidants.
Using the newly-developed assay, the scientists rated the ability of the non-diabetics to defend against free radical damage at 2.7, compared with 1.4 for those with microalbuminuria and 1.7 for the diabetics without microalbuminuria.
Though the exact mechanism of action of the oxygen free radicals is not yet clear, these findings confirm in humans earlier animal studies of the chemicals' role in damage in diabetes, Opara said. Previous Duke studies by Opara have shown that vitamin E can delay the development of diabetes in obese rats with Type II diabetes and that the depletion of the antioxidant glutathione caused diabetes in another rat model.
"The results we've been seeing in our animal studies are now being borne out in humans,” Opara said. "I recommend that since the body has many antioxidants, diabetics should take a number of these agents, including vitamins C and E and N-acetylcysteine."
The diabetic patients involved in the current study come from Egypt, and their samples were brought to Duke by E. Abdel-Rahman, one of Opara's collaborators.
Beta Carotene Prevents Prostate CancerHigh dietary consumption of beta-carotene may help prevent prostate cancer, according to research presented here last month at the annual meeting of the American Society of Clinical Oncology.
For men with the lowest dietary intake of beta-carotene, supplements show some promise in preventing prostate cancer--although it is too soon to recommend widespread supplementation, said lead investigator Meir Stampfer, M.D., of Brigham and Women's Hospital and Harvard Medical School, both in Boston. Dr. Stampfer reported the latest results from the ongoing Physicians' Health Study of more than 22,000 U.S. doctors that began in 1982.
Many studies have linked foods rich in beta-carotene with a lower risk of lung and various other cancers. Supplements of the antioxidant, however, have not lived up to early expectations. In fact, last year's results from the Physicians' Health Study showed no reduced risk of any type of cancer among men taking 50 mg of beta-carotene every other day, when compared with men taking placebo.
In the latest analysis of that population, Dr. Stampfer and colleagues compared plasma levels of beta-carotene that were measured at baseline and 12 years later in a subgroup of 1,318 men in whom prostate cancer had developed during the study and 2,038 men who served as controls.
Plasma levels of beta-carotene reflect dietary consumption of the antioxidant vitamin, Dr. Stampfer said.
The researchers found that prostate cancer was 36% more likely to develop in men in the lowest quartile of beta-carotene at baseline than in men in the highest baseline quartile. Also, among study participants with the lowest baseline levels, those who supplemented appeared to have a 19% reduced risk of cancer, although the decrease was not statistically significant, Dr. Stampfer said.
Still, the researchers concluded that "these subgroup analyses are compatible with the possibility that beta-carotene supplementation reduces risk of prostate cancer among those with low baseline levels."
Eating a diet rich in fruits and vegetables, though, is well-known to contribute to better health, he said. Indeed, it may be some other component of foods rich in beta-carotene that protects against cancer, and not the beta-carotene itself, he added.
Derek Raghavan, M.D., chief of the division of solid tumor oncology at the Roswell Park Cancer Institute in Buffalo, N.Y., agreed, noting that men should not supplement their diets with beta-carotene in hopes of preventing prostate cancer.
An estimated 334,500 new cases of prostate cancer will be diagnosed in the United States this year, and about 41,800 men will die from the disease, according to the American Cancer Society, headquartered in Atlanta. The disease is the second leading cause of cancer death in American men. --J.S.
CO Q10 Prevents and Restores Heart FunctionsMaking Old Hearts Younger Coenzyme Q10: It may, indeed, be a time-reverser.
Coenzyme Q10 has become one of the better-researched and substantiated "vitamin" supplements. Hundreds of studies document the multiple life-extension benefits of this versatile nutrient, not only as a powerful antioxidant, but also in augmenting the action of other antioxidants such as and in preventing such diseases as heart disease, neurological decline with age, and even periodontal disease.
Making
Old Hearts
Younger
Coenzyme Q10: It may, indeed, be a time-reverser.
By Robert Van Kampler, M.D.
Heart attacks and other types of heart disease affect older people to a much greater extent than the young. Young hearts bounce back much better from stress and damage, even the stress of treatment itself. However, treatment with coenzyme Q10 is demonstrating its ability to radically improve the heart's ability to recover from disease and stress.
Scientists in Melbourne, Australia, are giving coenzyme Q10 to elderly people about to undergo cardiac surgery in a bid to make their old hearts younger. Dr. Franklin Rosenfeldt, head of cardiac surgical research at the Baker Institute, says he expects the treatment will make the hearts of people over the age of 70 perform as well as those of 30-year-olds.
Rosenfeldt believes CoQ10 will improve heart function in two ways. The antioxidant fights free radicals released at times of stress, such as during cardiac interventions (including angioplasty, thrombolysis, and surgery). It also improves the way cells convert oxygen and food to energy, strengthening the heart and making it beat more strongly.
People in their 70's and 80's are likely to be those who benefit most, and hence these are the first subjects of a current clinical trial. Rosenfeldt has already achieved good results in laboratory and animal trials.
"We are giving the patients CoQ10 for a week before surgery to build up the energy levels in their cells, and we are testing to see whether their recovery after surgery is better, whether their heart shows less damage, and whether cardiac tissue removed at the time has greater energy capacity and also can stand up to stress better," Rosenfeldt says.
The double-blinded study, which began last June, is being conducted in two phases, a preliminary study involving 60 patients this year and the main study next year. (A double-blind study is one in which neither the subjects nor the persons administering the treatment knows which treatment a subject is receiving.)
Rosenfeldt says the results of cardiac treatments in elderly patients are known to be inferior to those in the young. In fact, the early mortality for elderly patients after such episodes as myocardial infarction, angioplasty,
and cardiac surgery is up to three times greater than for younger patients. A possible reason is an age-related reduction in cellular energy transformation during the intervention, which may induce stress. Rosenfeldt expects to find that CoQ10 improves the response to this stress.
Several years ago he conducted a project in which he showed how aging rats respond to stress, and especially how their hearts respond. In treating both elderly (three years old, which is equivalent to an 80-year-old human) and young rats (six months old, equivalent to a 30-year-old human), Rosenfeldt demonstrated that young hearts recovered about 45% after stress, whereas elderly rats recovered only 18%. "There was a much poorer response to stress in elderly hearts," he noted.
In another test, conducted by Dr. Michael Rowland, Rosenfeldt and their colleagues, the rats were given CoQ10 or placebo for six weeks before the same tests were performed again. "In the senescent hearts," they noted, "pre-pacing cardiac work was 74% and oxygen consumption 66% of that in young hearts. CoQ10 was able to specifically protect the elderly hearts against stress. By comparison, the untreated senescent hearts showed reduced recovery compared with the young hearts. We concluded that senescent rat hearts have reduced baseline function and reduced tolerance to aerobic stress, compared with young hearts. By pre-treating the senescent hearts with CoQ10, the baseline function of the senescent myocardium and its tolerance to aerobic stress was greatly improved." This work has been accepted for publication in Cardiovascular Research.
That study was then repeated using human tissues. During open heart surgery, a small piece of tissue was removed from the heart to allow one of the tubes to be inserted for the heart/lung machine. Some of the tissue was tested in the laboratory, where it was put in an organ bath and allowed to contract in a fairly normal environment of oxygen to determine how much force it could generate. "We found we could have tissues from elderly patients or young patients and they all contracted quite well in the organ bath," Rosenfeldt notes.
In the next test, the tissue was subjected to stress in the form of ischemia (reduced blood flow), emulating the effects of a heart attack or cardiac surgery in the piece of tissue. This time, there was a large difference between recovery of the young tissue and elderly tissue, with the young tissue bouncing back by about 60%, but the older tissue recovering only about 40%.
However, when the tissues were incubated in the organ bath with CoQ10 and subjected to the same stress, the result was similar to that found in rats: the elderly tissues from patients aged more than 70 years recovered just as well as the young tissues.
Rosenfeldt said CoQ10 has the potential to improve energy production in mitochondria by bypassing defective components in the respiratory chain, as well as by reducing the effects of oxidative stress. CoQ10 has emerged as a serious candidate for therapeutic use in the amelioration of bioenergetic defects manifested in the elderly heart.
In aged human atrial myocardium-the middle and thickest layer of the heart wall, composed of cardiac muscle-both hypoxia (reduction of oxygen) and simulated ischemia in vitro reveal a reduced capacity to recover pre-stress contractile function, compared with younger tissue. Rosenfeldt found that the frequency of mitochondrial dna deletion may be a useful molecular marker of stress-dependent, age-linked loss of tissue function. However, pre-treatment in vitro with CoQ10 overcomes the reduced capacity of senescent myocardium to recover contractile function after simulated ischemia, compared with younger tissue. (CoQ10 content is decreased in aged myocardium, and this decrease may play a role in the reduced post-stress recovery of contractile function.)
Rosenfeldt presented this work at the inaugural meeting of the International Coenzyme Q10 Society in Boston last May.
In recent years, most of the clinical work with CoQ10 has centered on heart disease, mainly congestive heart failure but more recently as an adjunct to cardiac surgery. Congestive heart failure has been widely reported as being related to significantly low blood and tissue levels of CoQ10, and the severity of heart failure correlates with the severity of CoQ10 deficiency.
Several trials have compared the effect on heart function of giving CoQ10 or placebo, measured by echocardiography. The ejection fraction-the fraction of the blood pumped out of the heart with each beat-showed a gradual and sustained improvement with CoQ10. Moreover, patients reported a reduction in fatigue, difficult or labored breathing (dyspnea), chest pain, and palpitations. The most dramatic results were seen in patients who were started on CoQ10 soon after the onset of congestive heart failure, although those with more established disease also frequently showed clear improvement.
There have now been numerous studies in various countries detailing the use of coenzyme Q10 as a treatment in heart disease. The efficacy and safety of the treatment has been well-established, including in large trials. One study, by Baggio et al., which took place in Italy, involved almost 2,664 patients with heart failure.
A study by Greenberg and Frishman found that 150 mg of CoQ10 reduced the frequency of angina attacks by up to 46%, while improving the capacity for physical activity in those patients. That work was published in the Journal of Clinical Pharmacology in 1990.
A study by Sunamori et al. published in 1991 reported that pre-treatment with coenzyme Q10 minimized the myocardial injury caused by cardiac bypass surgery and improved heart function, compared with patients not pre-treated with CoQ10 (Cardiovascular Drugs and Therapy, 5, 297-300).
More recently, R.B. Singh, from the Heart Research Laboratory at the Medical Hospital and Research Center in Moradabad, India, told the inaugural conference of the International Coenzyme Q10 Association that, in a randomized double blind trial of 144 patients with acute myocardial infarction, coenzyme Q10 was seen to be associated with a significant reduction in angina pectoris, arrhythmias, and left ventricular dysfunction.
Nonfatal infarction and cardiac deaths also were significantly lower in the coenzyme Q10 group than in the control group.
The future may be bright. At the conference, Dr. Peter Langsjoen noted that we are now at the beginning of an exciting new chapter in the clinical application of CoQ10 due to the rapid increase in public awareness and interest, all stimulating further clinical trials.
History of A Miracle Supplement
Coenzyme Q10, formerly known as ubiquinone, is essentially a fat-soluble vitamin or vitamin-like substance. Present in small quantities in a large variety of foods, it also is synthesized in body tissues. It is involved in several key steps in the production of energy within a cell, and it also functions as an antioxidant, a feature that explains its clinical advantages. It has no known toxicity or side effects.
The antioxidant or free radical-quenching properties of CoQ10 allow it to reduce oxidative damage to tissues. Such properties explain the interest in it as a means of slowing aging and age-related degenerative diseases.
It was first isolated from beef heart mitochondria in 1957 by Dr. Frederick Crane from Wisconsin, and soon afterwards by Professor R.A. Morton in the United Kingdom, who isolated it in rat liver. It was Morton who gave it the name ubiquinone, meaning ubiquitous quinone. In 1958, CoQ10 was synthesized by scientists at the pharmaceutical company Merck & Co.
The first medical use of CoQ7, a related compound, was reported in the mid-1960's by Professor Yuichi Yamamura in Japan, who used it in the treatment of congestive heart failure. Soon afterwards, Mellors and Tappel demonstrated that reduced CoQ6 was an effective antioxidant. In 1972, there was a report by Italian Gian Paolo Littarru and the late Karl Folkers from the University of Texas at Austin of CoQ10 deficiency in heart disease in humans. (The suffix 6, 7 or 10, by the way, refers to a five-carbon hydrocarbon called an isoprene that is attached to the quinone derivative; in mammals, the quinone derivative coenzyme Q usually contains 10 such units...thus, CoQ10).
By the mid-1970's, extensive medical research into CoQ10 became possible after the Japanese perfected the technology to produce it in pure form in large quantities. A few years later, it became possible to measure CoQ10 in blood and tissue by means of high-performance liquid chromatography.
A detailed history of the development and use of CoQ10 was written by Dr. Peter H. Langsjoen in 1994. He concluded that the "clinical experience with CoQ10 in heart failure is nothing short of dramatic, and it is reasonable to believe that the entire field of medicine should be re-evaluated in light of this growing knowledge. We have only scratched the surface of the biomedical and clinical applications of CoQ10 and the associated fields of bioenergetics and free radical chemistry."
Antioxidants Reduce Heart DiseaseA new study by researchers at the federal Centers for Disease Control and Prevention (CDC) in Atlanta shows that persons taking multivitamins can benefit from combining them with antioxidant vitamins such as Vitamin E to help reduce risks from serious disease such as heart illness and stroke.
Mortality risk from heart disease and stroke was l5 percent lower for users who took a combination of the vitamins, the study showed.
The researchers said their data provides support for the proposition that antioxidant vitamins taken in conjunction with multivitamins can reduce death risk from heart disease and cardiovascular disease or stroke. Vitamin E has been found in numerous previous studies to be effective in preventing a wide array of diseases. In the Atlanta study, Vitamins E, C and A, all considered antioxidants, were studied.
In the study entitled "Multivitamin Use and Mortality in a Large Prospective Study," published in the American Journal of Epidemiology, five researchers from the Atlanta center reported on their research into causes of death among more than one million adults.
The researchers compared death rates for persons who used Vitamin E and other antioxidant vitamins in combination with multivitamins, for persons who used multivitamins alone, and for persons who used the antioxidant vitamins only with the death rates of those who didn't take any vitamins.
The results showed adults who used Vitamin E or other antioxidant vitamins in combination with their multivitamin had a l5 percent lower risk of dying from heart disease or stroke than those who did not take vitamins.
Margaret L. Watkins and her associates at the Atlanta Center called for further studies to examine the role of vitamins in lowering mortality risks. The researchers indicated they were concerned with data that shows male smokers facing higher cancer risks with certain vitamin intakes, and said additional study is needed on cancer. "No such associations were seen in women," the researchers reported.
Multivitamin and combination use showed minimal effect on cancer mortality in the study, the researchers said.
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Heart attacks and other types of heart disease affect older people to a much greater extent than the young. Young hearts bounce back much better from stress and damage, even the stress of treatment itself. However, treatment with 
