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Vitamin E Consumption and the Risk of Coronary Heart Disease

Chapter I
INTRODUCTION

1.1 BACKGROUND
In Modern Era, coronary heart disease is one of the most cause human dead. Probably, this disease kills the human who doesn’t’ care about their health. As we know, there are many factors that can produce coronary heart disease such as junk food, high cholesterol food, goat meat, etc… The manifestations of coronary heart disease are coronary atherosclerosis, ischemic heart disease, and finally heart failure. Atherosclerosis is the leading cause of death and disability in the developed world. Despite our familiarity with this disease, some of its fundamental characteristics remain poorly recognized and understood. Although many generalized or systemic risk factors predispose to its development, atherosclerosis affects various regions of the circulation preferentially and yields distinct clinical manifestations depending on the particular circulatory bed affected
Because of the long effect that can be happened, we should think factors that can prevent that disease. Usually, the way to prevent coronary heart disease is by not eating high cholesterol food, make some exercise and take some drugs to decrease high cholesterol in the blood. It is true that we should check our health to doctor in order to prevent coronary heart disease when our age has been reached 30 years old.
Today, beside of many ways that we can do to prevent coronary heart disease, the scientist had found new way decrease the risk factor by using vitamin E. Although Vitamin E had been known long time ago, the effect to the heart have been known latterly. We hope that by consumption vitamin E regularly can help to reduce the coronary heart disease.
This paper wants to tell that vitamin E can help reduce the coronary heart disease and other disease related to the heart.
1.2 PROBLEMS
Almost everyone knows that the way to cure coronary heart disease is by operation or by taking some drugs, but the using of vitamin E is not thought by some doctors. We know that in the fact, vitamin E can reduce the incidence of coronary heart disease. And for the questions is how much vitamin E helps the heart? How about the relationship between vitamin E and coronary heart disease? This is the questions that must we answer together in order to save many people from one of the silent killer in the world.

1.3 LIMITATIONS OF THE PROBLEMS
Due to the large topic that can be discussed about vitamin E and coronary heart disease, so I will make some limitation so that the topic won’t to big. For more specific, I will describe my problems into 5 parts:
1. What is vitamin E?
2. What is coronary heart disease?
3. How can we diagnose coronary heart disease?
4. What are the relationship between vitamin E and coronary heart disease?
5. How about the implementation of vitamin E in coronary heart disease?
1.4 OBJECTIVES
I hope this paper will help us to know about the relationship between vitamin E and coronary heart disease and also an advantage of consumption vitamin E. We can study the characteristic of vitamin E related to the heart. For the objectives of this paper are to find out about:
1. What vitamin E is
2. What coronary heart disease is
3. How we can diagnose coronary heart disease
4. Whether there is relationship between vitamin E and coronary heart disease
5. The implementation of vitamin E in coronary heart disease

1.5 METHODS OF WRITING
The methods I use are from literature study that I have searching from many sources, especially from the internet, textbook, and library research which give me more up to date and comprehensive information. To analysis the characteristic, I was helped by my friends and sometimes discuss with them in my home. There are many problems during making this paper, but the problems can be handled.

1.6 FRAME OF WRITING
Preface
Content
Chapter I. Introduction
I.1 Background
I.2 Problems
I.3 Limitation of The Problems
I.4 Objectives
I.5 Methods of writing
I.6 Frame of Writing
Chapter II. Vitamin E
II.1 What is VITAMIN E ?
II.2 How vitamin E being absorp and metabolite? II.3 How the requirement of vitamin E?
II.4 What food provides vitamin E?
II.5 What the dietary deficiency of vitamin E is?
II.6 Who is at risk for vitamin E deficiency?
II.7 What about using of vitamin E for the treatment?
II.8 What About The Toxicity?

Chapter III. Coronary Heart Disease
III.1 What is coronary heart disease?
III.2 The Anatomy of The Heart
III.3 Overview
III.4 Pathophysiology
III.5 What is Angina?
III.6 What are The Risk Factors of Angina?
III.7 What are the prevention of Coronary Heart Disease
Chapter IV. The Correlation Between Vitamin E and Coronary Heart Disease
Chapter V. Conclusion
Bibliography

CHAPTER II
VITAMIN E

2.1 What is VITAMIN E ?
Vitamin E is a collective name for a group of tocopherols and tocotrionols, the latter having an unsaturated sidechain. There are eight naturally occurring plant compounds with vitamin E activity. RRR-a tocopherol is the most active, while synthetic stereoisomers of vitamin E are less biologically active. Vitamin E acts as a chain-breaking antioxidant and is an efficient pyroxyl radical scavenger, which protects LDLs and polyunsaturated fats in membranes from oxidation. A network of other antioxidants (e.g., vitamin C, glutathione) and enzymes maintains vitamin E in a reduced state. Vitamin E also inhibits prostaglandin synthesis and the activities of protein kinase C and phospholipase A2.
2.2 How vitamin E being absorp and metabolite?
Absorption and Metabolism Vitamin E is a fat-soluble vitamin and requires all the processes needed for micelle formation to be absorbed. About 15 to 40% is absorbed passively from a single physiologic dose, and there is less efficient absorption at high doses. Polyunsaturated fat may inhibit absorption. Vitamin E is taken up from chylomicrons by the liver, and an hepatic a tocopherol transport protein is involved in intracellular vitamin E transport and incorporation into very low density lipoprotein (VLDL). The transport protein has particular affinity for the RRR isomeric form of a tocopherol; thus this natural isomer has the most biologic activity. In the circulation, vitamin E is bound to all lipoprotein classes and becomes widely distributed in tissues, with fat and muscle being the most important storage depots. Vitamin E metabolites are mainly excreted in feces, although some are also excreted in urine.
2.3 How about the requirement of vitamin E?
The RDA for vitamin E is currently 10 mg for adults. Additional vitamin E is recommended during pregnancy (12 mg/d) and lactation (14 mg/d). Vitamin E is widely distributed in the food supply. The RRR-a isomers are particularly high in sunflower oil, safflower oil, and wheat germ oil; g tocotrionols are notably present in soybean and corn oils. Vitamin E is also found in meats, nuts, and cereal grains, and small amounts are present in fruits and vegetables. Vitamin E pills containing doses of 50 to 1000 mg are ingested by a large fraction of the U.S. population. In the older literature, 1 IU of vitamin E is equal to 1 mg all-racemic a tocopherol acetate. Diets high in polyunsaturated fats may necessitate a slightly higher requirement for vitamin E.
2.4 What food provides vitamin E?
Vegetable oils, nuts, green leafy vegetables, and fortified cereals are common food sources of vitamin E in the United States (U.S.). Table 1, Selected Food Sources of Vitamin E, suggests many food sources of vitamin E [4]. Food values are listed in alpha-tocopherol equivalents (ATE) to account for the variation in biological activity of the different forms of vitamin E.

2.5 What is the dietary deficiency of vitamin E?
Dietary deficiency of vitamin E does not exist. Vitamin E deficiency is seen only in severe and prolonged malabsorptive diseases, such as celiac disease, or after small-intestinal resection, leading to short-bowel syndrome. Children with cystic fibrosis or prolonged cholestasis may develop vitamin E deficiency characterized by areflexia and hemolytic anemia. Children with abetalipoproteinemia cannot absorb or transport vitamin E and become deficient quite rapidly. A familial form of isolated vitamin E deficiency also exists, which is due to a defect in the a tocopherol transport protein. Vitamin E deficiency causes axonal degeneration of the large myelinated axons and results in posterior column and spinocerebellar symptoms. Peripheral neuropathy is initially characterized by areflexia, with progression to an ataxic gait, and by decreased vibration and position sensations. Ophthalmoplegia, skeletal myopathy, and pigmented retinopathy may also be features of vitamin E deficiency. The laboratory diagnosis of vitamin E deficiency is made on the basis of low blood levels of a tocopherol (<5 ug/mL, or <0.8 mg of a tocopherol per gram of total lipids).

2.6 Who is at risk for vitamin E deficiency?
Vitamin E deficiency is rare in humans. There are three specific situations when a vitamin E deficiency is likely to occur. Persons who cannot absorb dietary fat due to an inability to secrete bile or with rare disorders of fat metabolism are at risk of vitamin E deficiency.
individuals with rare genetic abnormalities in the alpha-tocopherol transfer protein are at risk of vitamin E deficiency and premature, very low birth weight infants (birth weights less than 1500 grams, or 3 pounds, 4 ounces) are at risk of vitamin E deficiency.
Blood levels of vitamin E may also be decreased with zinc deficiency. Vitamin E deficiency is usually characterized by neurological problems associated with nerve degeneration in hands and feet. These symptoms are also associated with other medical conditions. A physician can determine if they are the result of a vitamin E deficiency or are from another cause.

2.7 What about the using of vitamin E for the treatment?
Symptomatic vitamin E deficiency should be treated with 800 to 1200 mg of a tocopherol per day. Patients with abetalipoproteinemia may need as much as 5000 to 7000 mg/d. Children with symptomatic vitamin E deficiency should be treated with 400 mg/d orally of water-soluble esters; alternatively, 2 mg/kg per day may be administered intramuscularly. Vitamin E in high doses may protect against oxygen-induced retrolental fibroplasia and bronchopulmonary dysplasia in prematurity, as well as intraventricular hemorrhage of prematurity. Vitamin E has been suggested to increase sexual performance, to treat intermittent claudication, and to slow the aging process, but evidence for these properties is lacking. High doses (60 to 800 mg/d) of vitamin E have been shown in controlled trials to improve parameters of immune function, and there are two intervention studies showing that vitamin E at 400 to 800 mg/d may be protective against cardiovascular disease, possibly by inhibiting LDL oxidation. Also, supplemental intake of vitamin E (100 to 200 mg/d) has been associated with a decreased risk of cataracts.

2.8 What about the toxicity?
High doses of vitamin E (>800 mg/d) may reduce platelet aggregation and interfere with vitamin K metabolism and are therefore contraindicated in patients taking coumadin. Nausea, flatulence, and diarrhea have been reported at doses >1 g/d.

Chapter III
CORONARY HEART DISEASE

3.1 What is coronary heart disease?
Coronary heart disease (CHD), also called coronary artery disease (CAD) and atherosclerotic heart disease, is the end result of the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium (the muscle of the heart). While the symptoms and signs of coronary heart disease are noted in the advanced state of disease, most individuals with coronary heart disease show no evidence of disease for decades as the disease progresses before the first onset of symptoms, often a “sudden” heart attack, finally arise. After decades of progression, some of these atheromatous plaques may rupture and (along with the activation of the blood clotting system) start limiting blood flow to the heart muscle. The disease is the most common cause of sudden death. Most Common reason for death of Men or woman over 65 years of Age.

3.2 The Anatomy of The Heart

Fig. 3.1 The anatomy of the heart

The heart consists of 4 chambers: an atrium and a ventricle on the right, and an atrium and ventricle on the left. Blood returning to the heart from veins all over the body flows into the right atrium. From there the blood flows into the right ventricle, which pumps it out to the lungs for oxygenation. The oxygen-rich blood returns to the left atrium. From there the blood flows into the left ventricle, which pumps it at high pressure into the arteries. This entire process constitutes one heartbeat. The pumping, or contraction, of the left ventricle must be very powerful because that is what keeps the blood flowing throughout the body. The strength of the heart muscle depends on the oxygen and nutrient supply coming via the coronary arteries. These arteries are usually strong, elastic, and quite flexible.
The heart has 3 major coronary arteries. Two of these arteries arise from a common stem, called the left main coronary artery. The left main coronary artery supplies the left side of the heart. Its left anterior descending (LAD) branch supplies the front part of the heart. The left circumflex (LCX) branch supplies the left lateral and back side of the heart. Finally, the right coronary artery (RCA) is separate and supplies the right and the bottom parts of the heart.
As a child, the inner lining of the coronary arteries is quite smooth, allowing blood to flow easily. As a person ages, the cholesterol and calcium content in the walls of the coronary arteries increases, making them thicker and less elastic.
Unhealthy habits, such as a diet high in cholesterol and other fats, smoking, and lack of exercise accelerate the deposit of fat and calcium within the inner lining of coronary arteries.
This process is known as atherosclerosis, or hardening of the arteries. The deposits, or plaques, eventually obstruct the blood vessel, which begins to restrict blood flow.
Plaque is like a firm shell with a soft inner core containing cholesterol. As blood hits it during each heartbeat, the plaque may crack open and expose its inner cholesterol core, which promotes blood clotting. Clots may further reduce blood flow, causing severe pain (angina), or even block it all together.
3.3 Overview
Atherosclerotic heart disease can be thought of as a wide spectrum of disease of the heart. At one end of the spectrum is the asymptomatic individual with atheromatous streaks within the walls of the coronary arteries (the arteries of the heart). These streaks represent the early stage of atherosclerotic heart disease and do not obstruct the flow of blood. A coronary angiogram performed during this stage of disease may not show any evidence of coronary artery disease, because the lumen of the coronary artery has not decreased in caliber.
Over a period of many years, these streaks increase in thickness. While the atheromatous plaques initially expand into the walls of the

Fig 3.2 Heart Attack Pathophysiology
arteries, eventually they will expand into the lumen of the vessel, affecting the flow of blood through the arteries. While it was originally believed that the growth of atheromatous plaques was a slow, gradual process, some recent evidence suggests that the gradual buildup of plaque may be complemented by small plaque ruptures which cause the sudden increase in the plaque burden due to accumulation of thrombus material.
Atheromatous plaques that cause obstruction of less than 70 percent of the diameter of the vessel rarely cause symptoms of obstructive coronary artery disease. As the plaques grow in thickness and obstruct more than 70 percent of the diameter of the vessel, the individual develops symptoms of obstructive coronary artery disease. At this stage of the disease process, the patient can be said to have ischemic heart disease. The symptoms of ischemic heart disease are often first noted during times of increased workload of the heart. For instance, the first symptoms include exertional angina or decreased exercise tolerance.
As the degree of coronary artery disease progresses, there may be near-complete obstruction of the lumen of the coronary artery, severely restricting the flow of oxygen-carrying blood to the myocardium. Individuals with this degree of coronary heart disease typically have suffered from one or more myocardial infarctions (heart attacks), and may have signs and symptoms of chronic coronary ischemia, including symptoms of angina at rest and flash pulmonary edema.
A distinction should be made between myocardial ischemia and myocardial infarction. Ischemia means that the amount of oxygen supplied to the tissue is inadequate to supply the needs of the tissue. When the myocardium becomes ischemic, it does not function optimally. When a large area of the myocardium becomes ischemic, there can be impairment in the relaxation and contraction of the myocardium. If the blood flow to the tissue is improved, myocardial ischemia can be reversed. Infarction means that the tissue has undergone irreversible death due to lack of sufficient oxygen-rich blood.
An individual may develop a rupture of an atheromatous plaque at any stage of the spectrum of coronary heart disease. The acute rupture of a plaque may lead to an acute myocardial infarction (heart attack). It is unclear at present which plaques in an individual are more likely to rupture in the future and cause a heart attack.

3.4 Pathophysiology
Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the myocardial cells. When myocardial cells die from lack of oxygen, this is called a myocardial infarction (commonly called a heart attack). It leads to heart muscle
Fig 3.3 The Picture of Plaque Location
damage, heart muscle death and later scarring without heart muscle regrowth.
Myocardial infarction usually results from the sudden occlusion of a coronary artery when a plaque ruptures, activating the clotting system and atheroma-clot interaction fills the lumen of the artery to the point of sudden closure. The typical narrowing of the lumen of the heart artery before sudden closure is typically 20%, according to clinical research completed in the late 1990s and using IVUS examinations within 6 months prior to a heart attack. High grade stenoses as such exceeding 75% blockage, such as detected by stress testing, were found to be responsible for only 14% of acute heart attacks the rest being due to plaque rupture/ spasm. The events leading up to plaque rupture are only partially understood. Myocardial infarction is also caused, far less commonly, by spasm of the artery wall occluding the lumen, a condition also associated with atheromatous plaque and CHD.
CHD is associated with smoking, obesity, hypertension and a chronic sub-clinical lack of vitamin C. A family history of CHD is one of the strongest predictors of CHD. Screening for CHD includes evaluating homocysteine levels, high-density and low-density lipoprotein (cholesterol) levels and triglyceride levels.
3.5 What is Angina?
The pain associated with very advanced CHD is known as angina, and usually presents as a sensation of pressure in the chest, arm pain, jaw pain, and other forms of discomfort. The word discomfort is preferred over the word pain for describing the sensation of angina, because it varies considerably among individuals in character and intensity and most people do not perceive angina as painful, unless it is severe. There is evidence that angina and CHD present differently in women and men.
Angina that occurs regularly with activity, upon awakening, or at other predictable times is termed stable angina and is associated with
Fig. 3.4 The Picture Angina Pectoris’ Attack

high grade narrowings of the heart arteries. The symptoms of angina are often treated with nitrate preparations such as nitroglycerin, which come in short-acting and long-acting forms, and may be administered transdermally, sublingually or orally. Many other more effective treatments, especially of the underlying atheromatous disease, have been developed.

Fig. 3.5 Angina Pectoris attack
Angina that changes in intensity, character or frequency is termed unstable. Unstable angina may precede myocardial infarction, and requires urgent medical attention. It is treated with oxygen, intravenous nitroglycerin, and morphine. Interventional procedures such as angioplasty may be done.

3.6 What are the risk factors?
The following are confirmed independent risk factors for the development of CAD, in order of decreasing importance:
1.Hypercholesterolemia (specifically, serum LDL concentrations)
2.Smoking
3.Hypertension (high systolic pressure seems to be most significant in this regard)
4.Hyperglycemia (due to diabetes mellitus or otherwise)
5. Hereditary differences in such diverse aspects as lipoprotein structure and that of their associated receptors, homocysteine processing/metabolism, etc.
Significant, but indirect risk factors include:
1.Lack of exercise
2.Stress
3.Diet rich in saturated fats
4.Diet low in antioxidants
5.Obesity
6.Men or Women over 65

3.7 Prevention
Coronary heart disease is the most common form of heart disease in the Western world. Prevention centers on the modifiable risk factors, which include decreasing cholesterol levels, addressing obesity and hypertension, avoiding a sedentary lifestyle, making healthy dietary choices, and stopping smoking. There is some evidence that lowering uric acid and homocysteine levels may contribute. In diabetes mellitus, there is little evidence that blood sugar control actually improves cardiac risk. Some recommend a diet rich in omega-3 fatty acids and vitamin C.
An increasingly growing number of other physiological markers and homeostatic mechanisms are currently under scientific investigation. Among these markers are low density lipoprotein and asymmetric dimethylarginine. Patients with CHD and those trying to prevent CHD are advised to avoid fats that are readily oxidized (e.g., saturated fats and trans-fats), limit carbohydrates and processed sugars to reduce production of Low density lipoproteins while increasing High density lipoproteins, keeping blood pressure normal, exercise and stop smoking. These measures limit the progression of the disease. Recent studies have shown that dramatic reduction in LDL levels can cause mild regression of coronary heart disease.
Risk factor management is carried out during cardiac rehabilitation, a 4-phase process beginning in hospital after MI, angioplasty or heart surgery and continuing for a minimum of three months. Exercise is a main component of cardiac rehabilitation along with diet, smoking cessation and blood pressure and cholesterol management.
Preventive diets
Vegetarian diet: Vegetarians have been shown to have a 24% reduced risk of dying of heart disease.
Cretan Mediterranean-style diet: The Seven Country Study found that Cretan men had exceptionally low death rates from heart disease, despite moderate to high intake of fat. The Cretan diet is similar to other traditional Mediterranean diets: consisting mostly of olive oil, bread, abundant fruit and vegetables, a moderate amount of wine and a small amount of animal products. However, the Cretan diet consisted of less fish and wine consumption than some other Mediterranean-style diets, such as the diet in Corfu, another region of Greece, which had higher death rates.
A study published in 2005 has determined that a positive relationship exists between the consumption of trans fat (commonly found in hydrogenated products such as margarine) and the development of endothelial dysfunction, a precursor to atherosclerosis.

CHAPTER IV
THE CORRELATION BETWEEN VITAMIN E AND CORONARY HEART DISEASE

We have known that Vitamin E, also known as tocopherol, is a fat-soluble vitamin. One of the roles fat plays in the diet is to transport fat-soluble vitamins. So Vitamin E is carried through the body attached to fat. The body stores vitamin E in fat deposits and in the liver.
Much research has focused on the role vitamin E may play in the prevention of heart disease because of its cancer artery and heart disease, vitamins C and E, and selenium are the antioxidants that have been studied the most antioxidant properties. Antioxidants are believed to be helpful in preventing heart disease.
Vitamin E’s role in heart disease prevention is not completely understood. Scientists believe that it may protect artery walls from the build up of plaque. It may help to strengthen blood vessel walls. It may also reduce LDL, known as the “bad” cholesterol, and increase HDL, known as the “good” cholesterol. Vitamin E also has mild blood-thinning properties. This may keep platelets, the parts of the blood that enable the blood to clot, from sticking together and also protect arteries.
Other studies from the National Heart, Lung, and Blood Institute are trying to pinpoint how much antioxidant we need for health benefits. Antioxidants such as vitamin C and selenium work with vitamin E to protect the body.
Additional diet and lifestyle factors are also key factors in cutting the risk of heart disease. There should also be a balance between the intake of vitamins and minerals. Too much of one vitamin can cause imbalances in the amounts of other vitamins in the body. Groups including the American Heart Association and the American Dietetics Association continue to recommend a balanced diet as the first step toward disease prevention, with antioxidant-rich foods such as:
1. fresh fruits, such as oranges, grapefruits, and strawberries
2. fresh vegetables, including broccoli, sweet potatoes, Brussels sprouts, and spinach whole grains
Vitamin E supplementation:
* reduces the oxygen requirement of tissues.
* gradually melts fresh clots, and prevents embolism.
* improves collateral circulation.
* prevents scar contraction as wounds heal.
* decreases the insulin requirement in about one-forth of diabetics.
* stimulates muscle power.
* preserves capillary walls.
* reduces C-reactive protein and other markers of inflammation
* Epidemiological evidence also suggests that a daily supplement of vitamin E can reduce the risk of developing prostate cancer and Alzheimer’s disease.
Other researches have found about vitamin E. They found that no benefit to heart disease from increased intake of vitamin E. These conflicting reports support the need for further research. But now, we can still using vitamin E safely and that issue has been proved. The clearest recommendation is that people should consult their doctors before starting to take high doses of any vitamin. This is especially true for people taking blood-thinning medicines, such as aspirin, warfarin sodium, or coumadin.

Low-dosage vitamin E supplementation (50 IU/d) decreases the risk of angina in patients without previously diagnosed CAD. Another study, using high-dosage vitamin E supplementation (400 or 800 IU/d), demonstrated a decrease in the combined end point of nonfatal myocardial infarction and cardiovascular death in patients with established CAD. Discordant data, however, have been published that imply no cardiovascular benefit of low-dosage vitamin E supplementation (50 IU/d) and detrimental effects if vitamin E is combined with beta carotene. At this point, clinicians should emphasize a low-fat diet with high intake of fruits and vegetable sources containing vitamin E. Supplemental vitamin E may be considered in patients at high risk for CAD or with documented CAD, but the potential beneficial effects should be weighed against possible long-term adverse effects. If vitamin E supplementation is initiated, the literature suggests dosages of 100 to 400 IU/d, with the higher dosage considered in patients with documented CAD.

CHAPTER V
CONCLUSION

After read all about the information of vitamin E, I can conclude that vitamin E play important role in coronary heart disease for therapy. We know that vitamin E is an antioxidant which protects artery walls from the build up of plaque. Vitamin E also helps to strengthen blood vessel walls. It may also reduce LDL, known as the “bad” cholesterol, and increase HDL, known as the “good” cholesterol. Vitamin E also has mild blood-thinning properties. This may keep platelets, the parts of the blood that enable the blood to clot, from sticking together and also protect arteries.
The dosage recommendation for this therapy is with high dose which mean that there may be a side effect that affect our body because we know that vitamin E is a fat soluble, so we must be careful when using vitamin E as a therapy. The Board has set an upper level of 1,000 mg for alpha-tocopherol . Upper levels are not the recommended amount to take. They are the maximum amount of a vitamin or mineral that can be taken safely without causing health problems. People should not routinely go above the set upper levels for any vitamin or mineral. Very large doses can lead to health problems instead of providing health benefits. Too much vitamin E can interfere with blood clotting and increase a person’s bleeding time to harmful levels. The patients, who eat vitamin E, must be under care to a physician.
I think it’s a good solution and can be tried to the patient with coronary heart disease. And for the research publication that hasn’t been proved, we should be careful of using high vitamin E dosage and report to the medical center if there were bad cases happened.

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