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“All truth passes through three stages. First, it is ridiculed. Second, it is violently opposed. Third, it is accepted as being self-evident.” Arthur Schopenhauer (1788 – 1860) What is the unfeigned cause of heart disease, and how may we genuinely reduce the peril of death? Atherosclerosis, or Coronary Artery Disease (CAD), is the leading cause of death in both men and women. In the U.S. alone, there are more than one million heart attacks each year, one third of them resulting in death. The majority of men and women presently have, or are actively developing, atherosclerosis. By age 20, most persons already have a 15-25% narrowing of their arteries due to plaque formation. By age 40, there is a 30-50% clogging of their arteries. In the beginning of the Twentieth Century, congestive heart sickness (CHD) was largely a result of rheumatic fever, which was a childhood disease. However by the year 1936 there was a dramatic change in the main cause of heart disease. Cardiovascular sickness caused by atherosclerosis, or plaque buildup, took primary place as the indispensable cause of heart disease, making congestive heart failure a distant second. During the 1950′s, the autopsies conducted on men who passed from physical life of heart impairment of normal physiological function that revealed plaque-clogged arteries concluded that cholesterol was the cause of hardening of the arteries (atherosclerosis) and coronary artery disease. Cholesterol, not calcium, was considered the “cause” of heart disease, in spite of plaque consisting of 95% calcium and a comparatively little percentage of cholesterol. By 1956 there were 600,000 deaths yearly from heart impairment of normal physiological function in the U.S. Of those 600,000, 90% were caused by atherosclerosis, or clogged arteries. In less than 25 years, the number one cause of death in the U.S. had changed dramatically …from congestive heart disease to coronary artery disease. Because cholesterol was dubbed the “cause” of atherosclerosis, the venture to lower cholesterol by any means started out in earnest. Both the feed industry and the pharmaceutical industry seized upon this probability to cash in on a cholesterol-lowering venture by creating foods and drugs that would supposedly save lives. Diets, such as the Prudent Diet, were established to lower the amount of cholesterol intake from food. There was no doubt that both polyunsaturated oils and drugs scaled down cholesterol, but by 1966 it was also apparent that letting down cholesterol did not translate into a scaled down risk of death from heart disease. As there was so much cash to be made from pharmaceutical development, the venture to formulate cholesterol-lowering drugs kicked into high gear, in spite of the lack of proof showing that the letting down cholesterol scaled down the danger of untimely death from heart disease. Heart impairment of normal physiological function kills 725,000 Americans annually, with women accounting for 2/3 or almost 500,000 of those deaths. After thirty years of cholesterol-lowering medications’ failure to significantly lower the death rate from cardiovascular disease, in 1987 a new and more dangerous class of drugs was unleashed upon the world: the “statin” drugs. Cholesterol-lowering statin drugs are now the ordinary of care that physicians are indoctrinated into prescribing to reduce cardiovascular disease. Are statin drugs the best way to prevent heart attacks and death? Before 1936 the most mutual type of heart impairment of normal physiological function was congestive heart sickness (CHD). It seldom caused sudden death and could be treated with the drug digitalis. The incidence of CHD remained stable until 1987, after which the incidence of the disease skyrocketed. Interestingly, the timing of the increased incidence of congestive heart disease coincides with the introduction of cholesterol-lowering statin drugs. Could cholesterol-lowering statin drugs have something to do with the weakening of heart muscles and the increased incidence of congestive heart failure? We will see that letting down the body’s co-enzyme Q10 levels, a side effect of statin drugs, does in truth increase the peril of muscle damage, including the muscles of the heart. Atherosclerosis is a impairment of normal physiological function characterized mainly by inflammation of the arterial lining caused by oxidative harm from homocysteine, a toxic amino acid intermediary found in everyone. Homocsyteine, in combining with other free radicals and toxins, oxidizes arteries, LDL cholesterol, and triglycerides, which in turn releases C Reactive Protein (CRP) from the liver-a marker of an inflammatory response within the arteries. Inflammation (oxidation) is the beginning of plaque buildup and ultimately, cardiovascular disease. Plaque, combined with the thickening of arterial smooth muscles, arterial spasms, and clotting, puts a person at a high peril of suffering heart attack or stroke. For years, doctors have hyper-focused on cholesterol levels. First it was the total cholesterol; later the focus became the symmetry of “good” HDL cholesterol to “bad” LDL cholesterol. In other words, how much of your cholesterol was good, and how much was bad? Of the two, the indispensable parameter is the level of HDL cholesterol, not LDL cholesterol. HDL, or high-density lipoprotein cholesterol, is responsible for clearing out the LDL cholesterol that sticks to arterial walls. Exercise, vitamins, minerals, and other antioxidants, specially the bioflavonoid and olive polyphenol antioxidants, increase HDL cholesterol levels and protect the LDL cholesterol from oxidative damage, and accordingly do more to reduce the risk of heart sickness than any medication ever could. There is not one thing inherent bad when it comes to LDL cholesterol. LDL cholesterol is critical to maintain life. LDL cholesterol only becomes “bad” when it is damaged, or oxidized by free radicals. Only the damaged, or oxidized form of LDL cholesterol sticks to the arterial walls to initiate the formation of plaque. Let us look towards cigarette smoking for a simple example demonstrating that we actually need to reduce oxidized LDL cholesterol to prevent atherosclerosis, as opposed to indiscriminately letting down LDL cholesterol with statin drugs. Everyone knows that cigarette smoking increments the danger of galore chronic diseases, such as cancer, heart disease, and stroke. Smokers with normal levels of LDL cholesterol are at an even more outstanding danger of devising heart impairment of normal physiological function than a non-smoker who has elevated levels of LDL cholesterol. Of course the reason why a smoker with normal levels of LDL cholesterol is at more outstanding risk of impairment of normal physiological function is because his LDL gets excessively oxidized. Cigarette smoke releases so a great deal of toxins and free radicals that the LDL cholesterol, the triglycerides, and the arterial walls are extensive oxidized. Homocysteine levels are also increased by cigarette smoking which further oxidizes LDL cholesterol and the arterial lining. Oxidation is the initiating cause of atherosclerosis. Therefore, the more and longer one smokes, the more oxidative harm he sustains and the dandier his peril of formulating heart disease. The degree of oxidation directly corresponds to the danger of heart disease. If you are not taking vitamins, minerals, and antioxidants then your LDL cholesterol is being oxidized, it is sticking to your arterial walls, and you ARE fabricating heart impairment of normal physiological function EVEN IF YOUR CHOLESTEROL LEVELS ARE NORMAL! LDL cholesterol starts sticking to arterial walls before the age of 5. Among the some free radicals that harm cholesterol, triglycerides and the arterial lining is homocysteine, a toxic intermediate biochemical devised for the duration of the conversion of the amino acid methionine into another necessary amino acid, cysteine. Both methionine and cysteine are non-toxic, but homocysteine is very toxic to the lining of the arterial endothelium. Homocysteine oxidizes LDL cholesterol, triglycerides and the arterial lining. Homocysteine is an amino acid normally invented in little amounts from the amino acid methionine. The normal role of homocysteine in the body is to control growth and help bone and tissue formation. However a problem arises when homocysteine levels in the body are elevated, causing exuberant harm to LDL cholesterol, as well as to arteries. Furthermore, homocysteine genuinely stimulates growth of arteriosclerotic plaque, which leads to heart disease. Thyroid hormone controls the level of homocysteine, but a good deal of elements play a role in the elevation of homocysteine. Normal aging, kidney failure, smoking, a lot of medications, and industrial toxins all elevate homocysteine levels. Interestingly, estrogen helps lower homocysteine. Homocysteine becomes elevated in the blood with a deficiency of the B vitamins-B6, B12 and folic acid. Genetics also play a role. About 12% of the population has an undetected defect calling for higher levels of folic acid than the rest of population to support maintain homocysteine levels in a safe range (below 6.5). Therefore if you have high homocysteine levels (> 7.0) even even though you are taking supplemental B complex vitamins, then you may be amid the 12% who need more than 1000 mcg of folic acid per day. In addition, betaine, likewise known as trimethylglycine (TMG) lowers homocysteine. Homocysteine is second only to cigarette smoking in it is oxidative destruction. It causes little nicks or tears in the arterial lining, while also oxidizing and detrimental LDL cholesterol. The damaged, or oxidized LDL cholesterol sticks to the homocysteine-damaged areas of the arterial lining. The combining of oxidized LDL cholesterol and a damaged arterial lining is what causes LDL cholesterol to stick to the arteries, whether or not the LDL cholesterol level is normal. Cholesterol-lowering statin drugs are the frequent for treating high cholesterol. This is dogma, and any individual who states other than as supposed or expected is committing medical heresy. Many humans find it hard to believe that pharmaceutical companies could ever succeed in paying medical researchers, medical associations, and doctors to commend something detrimental to our health. Most people do not recognise that pharmaceutical companies fund medical institutions, medical education, medical conferences, and still reward doctors and exploration originations for supplying favorable results on their drugs. Likewise, pharmaceutical companies often suppress negative results from studies done on their drugs. Money has the power to sweep negative results and severe side effects beneath the rug. Money has the power to influence the FDA to determine which drugs make it to market and which drugs become the “standard” of treatment. Former editor of the New England Journal of Medicine (NEJM), Dr. Marcia Angell, cautioned of the problem of commercializing scientific exploration in her outgoing editorial titled “Is Academic Medicine for Sale?” Angell called for more inviolable limitations on pharmaceutical stock ownership and other financial incentives for researchers. She said that growing conflicts of interest were tainting science, warning “When the boundaries amidst industry and academic medicine become as blurred as they are now, the business goals of industry influence the mission of medical schools in multiple ways.” She did not discount the gains of exploration but said, “a Faustian bargain” now existed amongst medical schools and the pharmaceutical industry. Angell left the NEJM in June 2000 and has written a book, “The Truth About the Drug Companies: How They Deceive Us and What to Do About It.” Two years later, in June 2002, the NEJM declared that it was going to commence accepting articles that were written by biased researchers, as there weren’t sufficient unbiased researchers left to write articles. In other words, most exploration originations were now financed by one or more of the a lot of pharmaceutical companies. An ABC report noted that a survey of clinical tryouts revealed that when a drug company did not fund a study, favorable results when it comes to a drug were found only 50% of the time. In studies furnished by drug companies favorable results regarding the drugs were reported an awful 90% of the time. Money may and does buy the desired results. This is how most medical exploration and drugs are now devised and brought to market. In 1977, the internationally-renowned heart surgeon, Dr. Michael DeBakey pointed out that only 30-40% of people with blocked arteries and heart disease have elevated blood cholesterol levels, and posed the logical question, “How do you explain the other 60-70%?” Because letting down cholesterol did not reduce the danger of death from heart disease, the Cholesterol Consensus Conference in 1984 invented new guidelines to lower the “acceptable level” of cholesterol. High cholesterol would now be the diagnosis for any man or woman with a cholesterol level over 200. Doctors had to convince their persons who requires medical care that they had the sickness and necessitated to take one or more highpriced drugs for the rest of their lives. However, when letting down total cholesterol levels under 200 did not translate into saving lives from heart attacks, the focus then turned to LDL cholesterol levels. The “disease” of high cholesterol was refined to the impairment of normal physiological function of high LDL cholesterol. The adverse patient who had an LDL cholesterol level above 130 was now condemned to a lifetime of highpriced drugs. Though wholly illogical, even when a person with normal LDL cholesterol levels suffered a heart attack, he would still be prescribed a cholesterol-lowering drug. As we shall see, statin drugs reduce the risk of death by repeat heart attacks by as much as 30%, but interestingly enough, the mechanism of action in reducing the risk of death after a heart attack is not thru statin drugs’ capacity to lower cholesterol! It has been ran into that statin drugs have a modest anti-inflammatory and antioxidant effect. Yet, there are some natural antioxidants that reduce inflammation and oxidation of LDL cholesterol and the lining of the arteries, which may soon be encountered to be more effective in reducing the danger of death than “antioxidant drugs,” without toxic side effects. The myth that high LDL cholesterol is the crucial cause of heart disease, and that we must be on drugs to protect ourselves is dispelled by the evidence. If the premise were unfeigned that humans with high levels of LDL cholesterol get heart disease, then we could assume that people with normal levels of LDL will have to not get heart disease, or at least very few must get it. However, as Dr. DeBakey observed, approximately 60% of those who die from heart disease have normal LDL cholesterol levels! Furthermore, after over 45 years of doctors prescribing cholesterol-lowering drugs, heart impairment of normal physiological function and stroke still stay the number one cause of death in both women and men. This says that irrespective of whether you have a high or a normal level of cholesterol, you have a 50% chance of dying from heart disease. If this is so, and it is, then why take a dangerous drug to undertake to lower your cholesterol in the initial place? In 2001, the target level of LDL cholesterol was lowered from 130 to 100, and during one night the number of humans considered to be nominees for cholesterol statin drugs doubled. Many persons such as myself bristled at the news, because we knew the effectiveness of vitamins, minerals, and antioxidants in preventing and reversing heart disease. Many of us could see the conspiracy for what it was. The level at which LDL cholesterol is considered normal has continually been influenced by pharmaceutical companies, who pull the financial strings of exploration grants that keep medical schools and medical organizations in business. The lower they may establish the level at which LDL cholesterol is considered to be normal, the more persons mechanically become victims of the dreaded sickness of “high cholesterol.” Therefore, more people will be persuaded that they need to be taking a statin drug, and voilà, more net income for the manufacturers. When you consider the size of the profits already received, let alone the potential earnings from statin drugs over the next various years, the cholesterol conspiracy is one of the biggest cash making systems ever perpetrated on the world. In July 2004, the level of LDL cholesterol considered normal underwent another change. The new norm plunged from 100 to 70, almost doubling again the number of humans who are “infected” with the plague of high cholesterol. Why, it’s the epidemic of our time! Many enlightened humans howled at this news, marveling if the masses would ever wake up and see who is behind this, and why. Why is the medical institution ignoring the thousands of published medical studies that show the beneficial effects of nutritional supplements versus heart disease? Why is the medical institution down-playing the dangerous and deadly side effects of statin drugs? The “updated” LDL cholesterol recommendations were published in the July 2004 issue of the American Heart Association’s publication, Circulation. A panel from the National Heart, Lung and Blood Institute, a section of the National Institutes of Health, which is endorsed by the American College of Cardiology, and the American Heart Association, were the ones who genuinely pronounced the new cholesterol level at which drugs will have to be prescribed. Sounds beauteous official and dependable if these powerful medical originations are backing up these recommendations, right? The fact is eight of the nine panel members making the new LDL cholesterol recommendations were being paid by the statin-producing pharmaceutical companies. The panelists did not disclose their financial conflict of interest. This info was uncovered by Newsday, a Long Island, New York You would think that with all the publicity and recommendations from medical experts on the gains of statin drugs, the medical community would possess overpowering proof that the drugs reduce the risk of death from cardiovascular disease. A hint of galore of the smoke and mirrors in the pharmaceutical companies’ advertizing may be seen in their TV commercials. Read cautiously the little print on numerous of Crestor’s® mercantile advertising. Their mercantile states how much it lowers LDL cholesterol. However, in the same ad you may read, “…Crestor® has not been shown to reduce the peril of heart sickness or heart attack.” If so, then why take it? Isn’t the bottom line to prevent death? The scheme for reporting averse effects from medications is tremendously flawed, so much so that a good deal of persons are badly harmed or killed by a lot of medications before they are at last got rid of from the market. Most doctors do not recognise what sensations or changes or effects are due to the drug, what ought to be reported, or even to whom to report averse effects. They assume that the exploration that went into formulating the drug has already identified all the effects and that a drug brought to market is “safe.” However, only one in twenty side effects is ever reported to either hospital administrators or the FDA. Statin drugs block cholesterol production in the body by inhibiting the enzyme called HMG-CoA reductase in the early steps of it is synthesis in the mevalonate pathway. Cholesterol is one of three end productions in the mevalonate chain. This same biosynthetic pathway is also applied to give rise to co-enzyme Q10, or co-Q10, as well as dilochol. Therefore, one ominous consequence of statin drugs is the unintentional inhibition of both Co-Q10 and dilochol synthesis. The drug info insert of a statin drug states that it lowers co-enzyme Q10 levels. Most doctors have forgotten their biochemistry class in medical school, and forgotten when it comes to the importance of Co-Q10. Therefore they apparently are not concerned regarding such a statement on the drug labeling selective information sheet. They may even reassure their people who are in need of medical care that letting down Co-Q10 is not one thing to worry about, but at the same time warn them that the drug may cause liver harm and to have their liver enzymes checked each three to six months to make sure the drug isn’t killing them. They do not realize that it is the depletion of Co-Q10 that leads to liver harm and death. Ubiquinone, or co-enzyme Q10, is a critical cellular nutrient developed in the cell’s mitochondria, the “engines” that fabricate energy for the cell. Mitochondria use sugar, oxygen, and water to manufacture energy molecules known as ATP. Without ATP cells could do nothing. Damaged tissues could not be repaired. Cells could not divide or formulate or utilise proteins, enzymes, or hormones. Death of cells, and in truth of the humane body would occur if ATP could no longer be produced and utilized. Co-Q10 functions within the mitochondria as an electron carrier to cytochrome oxidase, our main respitory enzyme, which helps turn oxygen and sugar into energy. The heart requires high levels of oxygen, sugar, and Co-Q10 since it utilizes a lot of energy. A form of Co-Q10 called ubiquinone is found in all cell membranes, where it plays a role in preserving membrane integrity, so critical to nerve conduction and muscle contraction. Co-Q10 is also critical for the formation of elastin and collagen, which make up the connective tissues of the skin, musculature, and the cardiovascular system. The most mutual side effect of statin drugs is muscle pain and weakness. In fact, numerous people who are in need of medical care who get started on the statin drugs almost without delay observe generalized fatigue and muscle weakness. This is due to the depletion of Co-Q10 necessitated to aid muscle function. Dr. Beatrice Golomb of San Diego, California, is presently conducting a series of studies on statin side effects. The pharmaceutical industry insists that only 2-3% of people who are in need of medical care get muscle aches and cramps, when in fact in one study, Golomb found that 98% of people who are in need of medical care taking Lipitor®, and one-third of the persons who requires medical care taking Mevacor® (a lower dose statin), suffered noticeable to substantial muscle problems. Some people on statin drugs lose coordination of their muscles. Some manufacture pain in their muscles, a heap of are not capable to write due to loss of fine motor skills. Many lose the strength to exercise. Others are falling more many times as their muscles give out, still others have trouble sleeping due to muscle cramping and twitching. Even worse, a heap of humans are experiencing most of these side effects. The difficultnesses are so numerous, it is difficult to list all the sensations or changes people might experience. These difficulties do not come from the “disease” of high cholesterol, but the sickness of ignorance in prescribing these drugs. As we age, Co-Q10 levels decline naturally. From the age of 20 to 80, Co-Q10 levels fall by almost 50%. Along with the natural decline of Co-Q10, comes a natural decrease in energy and an increase in the danger of heart disease, stroke, and cancer. If the natural decline of Co-Q10 levels increments the danger of fatigue, cancer, heart disease, and stroke, would it not make sense that accelerating the decline of Co-Q10 levels with statin drugs would have the same effect? They do indeed! Demonstrating the importance of Co-Q10 to cardiovascular health, in a randomized, double blind, placebo-controlled study of people either taking or not taking statin drugs, supplementation with Co-Q10 scaled down the risk of heart attacks and death in those with heart sickness and prior heart attacks by 50%, disregarding of whether they were on a statin drug or not. (Singh R, Neki N, Kartikey K, et al. Effect of coenzyme Q10 on risk of atherosclerosis in persons who requires medical care with recent myocardial infarction. Mol Cell Biochem. 2003 Apr; 246(1-2):75-82.) Additionally, Co-Q10 was shown to increase blood levels of vitamin E and significantly increase the levels of protective HDL. As low HDL is a major danger element for heart disease, increasing it is a definitive benefit. Statin drugs were shown not to provide any gain beyond that of supplementing with Co-Q10. Let me make this clear – in this study only the co-enzyme Q10 provided any benefit, not the drugs! Cardiologist Dr. Peter Langsjoen of East Texas University reported the effects of Lipitor® amongst 20 persons who requires medical care who started with exclusively normal hearts. After six months on a low dose of 20 mg of Lipitor® per day, two thirds of the persons who requires medical care started to show signs of heart failure, as seen by abnormalities in the heart’s filling phase. According to Dr. Langsjoen, this malfunction is due to Co-Q10 depletion. Nine controlled tryouts using statin drugs in persons have been conducted therefore far. Eight of these showed significant statin-induced Co-Q10 depletion leading to a decline in left ventricular function and other biochemical imbalances. In the United States, the incidence of heart attacks over the past ten to fifteen years has declined slightly. But congestive heart failure and cardiomyopathy have risen alarmingly. Is it a coincidence that statin drugs were original marketed in 1987, and then from 1989 to 1997, deaths from congestive heart failure more than doubled? 38 It frightens me that nearly all persons who requires medical care with heart failure are put on statin drugs, even if their cholesterol is already low. In my opinion, the worst thing to do for a failing heart is take a statin drug. The best thing is to take is a full range of quality nutritional supplements, …vitamins, minerals, fish oil, and other antioxidants, including Co-Q10. Various antioxidants work synergistically, each contributing to the fight versus free radicals in dissimilar areas and in dissimilar ways. In the blood stream, water-soluble antioxidants, such as vitamin C, and grape seed extract come in contact with and neutralize free radicals before they harm LDL-cholesterol. Other antioxidants saturate arterial walls and other tissues, and protect collagen and elastic fibers from free radical damage, reducing inflammation and plaque formation. The fat-soluble antioxidants, vitamin E, beta carotene, and co-enzyme Q10 ride along in the blood fat (triglycerides) and LDL cholesterol, protecting them and the endothelium from oxidation. Vitamin E sits on the surface of LDL cholesterol, protecting it from free radical damage. Beta carotene, grape seed extract and olive extract penetrate deeper inside the LDL cholesterol and arterial walls, adding more shelter from oxidation. Quercetin and alpha lipoic acid work through nitrous oxide pathways to reduce high blood pressure, a major danger factor for heart disease. A report published in the Archives of Internal Medicine in 2005 looked at 97 double-blind controlled studies comparing the efficacy of cholesterol-lowering statin drugs to fish oil. They found that cholesterol-lowering statin drugs scaled down the risk of death from heart sickness by only 13%, and Even more interesting, the salmon oil was shown to reduce the danger of death from heart impairment of normal physiological function by 23%, closely double the gain of statin drugs. Salmon oil is an omega-3 fatty acid that gets integrated into cholesterol and triglycerides and prevents the oxidation of LDL cholesterol. Since LDL cholesterol is protected from exuberant oxidation there is less plaque buildup and less peril of heart disease. Inflammation is a well-known factor in the formation of atherosclerosis. To keep it simple, think of inflammation and oxidation as the same process. The immune system’s response to inflammation is to The liver’s response to inflammation is to release C reactive protein (CRP) into the blood. Other inflammatory causes may cause elevated CRP levels, including cigarette smoking, obesity, insulin insensitivity, diabetes, rheumatoid arthritis, infections, dementia, colorectal cancer, high blood pressure, and aging. Accordingly, elevated CRP levels are a direct indication of inflammation in the body and that atherosclerosis, including heart disease, is actively developing. Homocysteine and high sensitivity CRP levels may and ought to be tested. Dr. Jialal, of the Universtity of Texas Southwestern Medical School at Dallas, is well known for his exploration correlating oxidized LDL cholesterol as the unfeigned cause of atherosclerosis, has likewise identified high sensitivity C reactive protein as a predictive danger element for inflammation of arterial walls and plaque formation. Your doctor may not test for these routinely, but you ought to insist on getting these tests done. Both of these predictive values may be kept at “safe” levels. Vitamins, minerals, antioxidants, and omega-3 fatty acids may lower the levels of homocysteine and CRP. The B vitamins, along with betaine, or tri-methyl-glycine (TMG), alter homocysteine into safer amino acids and reduce inflammation of the LDL cholesterol and the arterial lining. When you receive the results of your homocysteine test, do not receive the answer, “Your test was normal.” Ask for the actual number. The doctor and nurse commonly know what is normal by what the lab slip states as the “normal range.” Most lab results report a normal homocysteine level as being under 10.4, when in fact, since the early 1990′s, researchers have known that a homocysteine count above 6.5 signals a rapid linear rise in the danger for heart disease. Furthermore, with each 3 point elevation of homocysteine above 6.5, e.g., when homocysteine levels are 9.5, the danger of coronary artery impairment of normal physiological function (CAD) rises by an further and added 35%! Yet you may be told that 9.5 is “normal and not to worry.” With a homocysteine level of 12.5, the increase in the I need to emphasize that any individual whether they have a medical problem or not, will have to talk about this data with their physician before acting upon anything written here. The data provided is not meant to diagnose or treat any disease. It is for informational purposes only; and no one ought to make conclusions with regards to their medications without consulting with their physician. No one will have to come off a cholesterol-lowering statin drug in lieu of nutritional supplements without a exhaustive discussion with their physician who is keenly conscious of all the pros and cons of both treatment modalities. In summary, I commend a full spectrum of quality nutritional supplements, along with a healthful diet and exercise, to support obtain and maintain optimal heart and arterial health. I believe all would agree that life style changes are the most necessary factor for optimal health, …and some believe that quality nutritional supplements are key in protecting versus the procedure that leads to, and accelerates the development of closely all chronic degenerative diseases, that of oxidation. To combat oxidation we need a full range of quality antioxidants.
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