text:
Cardiovascular Disease
Cardiovascular disease is the general term for heart ("cardio") and blood vessel ("vascular") diseases. These include atherosclerosis, coronary heart disease, heart attack, stroke, high blood pressure, peripheral vascular diseases and congestive heart failure. Cardiovascular disease accounts for one in every two deaths in developed countries. Coronary heart disease causes 36% of all deaths in the US and is the number one killer disease. Stroke, another type of cardiovascular disease, is the third most common cause of death.
Causes of Cardiovascular Disease
Risk factors for cardiovascular disease include high cholesterol, smoking, high blood triglyceride levels, excess weight, stress, drinking too much alcohol and lack of exercise. Diabetics are also at increased risk of cardiovascular disease.
Heredity also plays a part in cardiovascular disease. Both men and women are more likely to develop heart disease if close blood relatives have had it. Screening, dietary intervention and possibly drugs may be useful in treating those in the early stages of disease. Being overweight in the first ten years of life also increases the risk of heart disease. The disorder is twice as likely to develop in those who are inactive as in those who are active.
Coronary heart disease strikes hardest at men in their mid-fifties. Men are more likely than women to suffer from heart attacks, and they also tend to have them earlier in life. However, after menopause more women die from heart attacks. Studies show that women's cholesterol is higher than men's from age 55 onwards.
The underlying cause of cardiovascular disease is atherosclerosis. The general term arteriosclerosis is used to describe the thickening and hardening of the arteries that occurs as people get older. Atherosclerosis occurs when deposits of fatty substances, cholesterol, cell waste products, calcium and fibrin (a clotting material from blood) build up in the inner lining of the artery. The build-up is known as plaque and as it increases bleeding can occur, eventually leading to the formation of blood clots. If a clot blocks a whole artery, a heart attack or stroke can occur.
The development of atherosclerosis can begin at a very early age and is usually not noticed until serious health problems such as a heart attack or stroke occur. About 13.5 million Americans know that they have the disease.
Atherosclerosis is a complex process and exactly how it begins or what causes it, is unknown. However, it seems likely that damage to the inner lining of blood vessels starts the process. Considerable evidence suggests that a high level of cholesterol is the most important factor contributing to the disease process. Certain types of cholesterol are vulnerable to oxidative damage by free radicals, and oxidized cholesterol is more damaging to arteries than unoxidized cholesterol. New research suggests that other compounds are also vulnerable to oxidation, including those in white blood cells known as macrophages, which can promote plaque formation by causing inflammation and the release of toxic substances that can damage cells.
Atherosclerosis can affect any area of the body. Blocked coronary arteries affect the heart, while narrowing of the carotid arteries of the neck may reduce mental functioning. Atherosclerosis of the leg arteries leads to intermittent claudication in which it is difficult to walk without pain; and clogging of the pelvic arteries affects sexual performance.
Coronary Heart Disease
The coronary arteries are those that supply blood to the heart. They are attached directly to the wall of the heart and are squeezed and expanded as the heart muscle contracts and relaxes. This contraction occurs 100 000 times a day, placing the coronary arteries under considerable stress and causing them to be especially vulnerable to damage and disease. Coronary heart disease is also known as ischemic heart disease and its most common forms are myocardial infarction (heart attack) and angina pectoris (chest pain).
Angina pectoris has symptoms of a squeezing or pressure-like chest pain, which usually occurs after physical exertion. The pain can be severe or mild and usually lasts from one to 20 minutes. Angina is caused by an insufficient supply of oxygen to the heart, usually because of the build-up of atherosclerotic plaque.
A special type of angina, known as variant angina, occurs when the coronary arteries go into spasm. This type of angina can occur at rest, at odd times during the day or night, and is more common in women under the age of 50.
Heart Attack
A heart attack occurs when the blood supply to the heart muscle is sharply reduced or stopped, after one of the coronary arteries is blocked. If the blood supply is cut off for a long period, death may result. About 1.5 million Americans suffer from a heart attack in any one year. Coronary artery disease, in which the arteries supplying blood to the heart become blocked by the build-up of atherosclerotic plaque, is the underlying cause of heart attacks.
Lifestyle changes such as stopping smoking, eating a healthy diet and an appropriate exercise program can help to prevent heart attacks, even in those who may have already suffered. Drug therapy including aspirin, ACE inhibitors, beta blockers and cholesterol-lowering drugs may also play a part. Hormone replacement therapy in postmenopausal women can also reduce the risk as estrogen protects the heart.
Risk Factors for Cardiovascular Disease
Cholesterol is a type of fat that has many vital functions in the body. It is part of cell membranes and is necessary for the manufacture of bile acids and many hormones. Cholesterol is manufactured in the body and is also found in foods of animal origin. Plant foods do not contain cholesterol.
As cholesterol is a fat-soluble molecule it cannot dissolve in the blood. It is therefore attached to compounds known as lipoproteins, which transport it to different places in the body. There are several types of lipoprotein cholesterol compounds. These include LDL (low density lipoprotein) cholesterol, which transports cholesterol to the tissues; and HDL (high density lipoprotein) cholesterol, which transports it to the liver for metabolism and excretion.
High levels of LDL cholesterol promote build-up in atherosclerotic plaques in the artery walls while HDL cholesterol reduces this. Hence LDL cholesterol is often referred to as bad cholesterol while HDL cholesterol is referred to as good cholesterol. The ratio of LDL to HDL cholesterol is an important factor in disease development as it determines whether cholesterol is being deposited into the arteries or taken to the liver to be excreted.
Cholesterol levels are influenced by genetic make up and by diet. For years it was thought that foods high in cholesterol raised blood cholesterol. Further research has shown that while high cholesterol foods can raise blood cholesterol levels, the saturated fat content of foods has a greater effect. It is currently recommended that total blood cholesterol should be less than 200 mg per deciliter of blood. LDL cholesterol should be less than 130 mg per deciliter and HDL cholesterol more than 35 mg per deciliter. At these levels, a person's risk of heart disease is low.
Recently, a compound called lipoprotein(a) or Lp(a) has been found to be an independent risk factor for heart disease. When Lp(a) levels are above 30 mg per deciliter, the risk of heart disease is increased. Lp(a) may act by delaying the breakdown of blood clots.
Triglycerides are the chemical form in which most fats exist in food and in the body. Calories not used by the body immediately are converted to triglycerides and transported to fat cells. Hormones regulate the release to meet energy needs between meals. An excess of triglycerides in the blood is linked to an increased risk of heart disease. It is currently recommended that triglyceride levels should be lower than 150 mg per deciliter.
Blood Platelets
Blood cell fragments known as platelets play an important role in the process of atherosclerosis. The gathering together or 'aggregation' of platelets is essential for the formation of blood clots in wound-healing. However, excessive platelet aggregation increases the risk of cardiovascular diseases such as heart attack and stroke. When platelets clump together around atherosclerotic plaques, they release compounds which cause the plaques to grow further and eventually block the artery. There are many chemicals in food which affect platelet function and these can either have beneficial or harmful effects depending on whether they increase or decrease aggregation.
High Homocysteine Levels
Several studies have found a link between high levels of a substance called homocysteine and cardiovascular disease. Homocysteine forms when the body breaks down protein. Enzymes either turn homocysteine back into the amino acid methionine, which can then be used to build protein, or break it down for excretion in the urine. High levels of homocysteine may be toxic to the cells that line blood vessels and may also increase the adhesiveness of platelets and other clotting factors.
Homocysteine levels are influenced by dietary intakes of folate, vitamin B6 and vitamin B12. They also vary according to race, gender, age and certain disease conditions. A dangerous cause of high blood pressure known as isolated systolic hypertension has also been found to be linked to homocysteine levels. Homocysteine may cause excessive stiffening of the aorta and other blood vessels thus forcing the heart to pump harder and thereby increasing the risk of heart and blood vessel diseases.
Being overweight increases the risk of cardiovascular disease by raising blood pressure, increasing blood fats, reducing HDL cholesterol and raising the risk of diabetes. This is particularly the case when the excess body fat is stored in the chest and abdomen.
Smoking increases the risk of cardiovascular disease. Smoking reduces the ability of the blood to deliver oxygen to the heart, stiffens arteries, damages blood vessel linings, promotes clotting, increases cholesterol levels and makes LDL cholesterol more susceptible to oxidative damage by free radicals. Even nonsmokers who live with heavy smokers have an increased risk of heart disease, and women may be more susceptible to the risks of smoking than men.
Stress increases the risk of heart disease and those who have high levels of hostility and unexpressed anger are also at higher risk. Sudden psychological stress may also trigger heart attacks. Depression also seems to be linked to heart disease, particularly new depression. Effective relaxation techniques such as meditation have been found to reduce stress and prevent heart attacks.
Preventing Cardiovascular Disease
Eating a healthy diet, not smoking, maintaining a healthy body weight, limiting alcohol consumption and practicing effective stress reduction techniques are very important in the prevention of cardiovascular disease. Exercise is also a vital part of any prevention program and many studies have shown reduced risk in men and women who exercise regularly. Exercise can reduce blood cholesterol, blood pressure and lead to a reduced risk of obesity and diabetes. Vigorous exercise is good for the heart, lungs and circulation. Activities such as brisk walking, jogging, cycling and swimming for at least 30 minutes three to four days per week at 50 to 75 per cent of maximum heart rate bring the most beneficial effects. For elderly people, moderate or low intensity exercise may be more suitable.
Diet and Cardiovascular Disease
The link between diet and cardiovascular disease is a strong one. Diets high in saturated fats, salt, cholesterol and sugar increase the risk of heart disease; and diets high in fresh fruit, vegetables and fiber decrease it. Many population studies show that a 'Mediterranean diet' that is high in olive oil, fresh and dried fruit, grains, legumes and nuts appears to lower both cholesterol levels and heart disease risk.
Fiber in the diet reduces the risk of heart disease. Daily intake should be around 35 grams. Fiber binds cholesterol and fats and lessens their absorption. It also decreases total and LDL cholesterol levels and increases protective HDL cholesterol levels. Results of studies such as the Physicians Health Study show that fewer heart attacks occur in those that eat more fiber, particularly the soluble type found in oat bran, fruit and vegetables.1
Reducing dietary fat has the greatest impact on lowering blood cholesterol and lowering the risk of cardiovascular disease. However, it is not only the amount of fat in the diet that affects the risk of heart disease, but also the type.
Saturated fats are found in animal foods such as meat, butter and cheese; and plant foods such as coconut oil and palm oil. Trans fats are unsaturated fats, which have undergone a chemical process called hydrogenation to turn them into saturated fats. They are found in packaged foods such as pastries, cookies, crackers and baked goods. High consumption of these fats increases cholesterol and triglyceride levels, and increases platelet aggregation. This contributes to atherosclerosis. Polyunsaturated fats which are found in oils of plant origin such as safflower, sesame, sunflower and corn may help to lower cholesterol and decrease platelet aggregation, thus reducing the risk of heart disease. However, polyunsaturated oils are susceptible to oxidation and may also lower HDL cholesterol. Monounsaturated fats such as those found in canola, olive and peanut oils may also help to lower cholesterol and decrease platelet aggregation. They are also less susceptible to oxidation. Adequate intakes of the essential fatty acids are important in the prevention of heart disease.
The results of a 1997 study published in the New England Journal of Medicine suggest that replacing saturated and trans-unsaturated fats with unhydrogenated monounsaturated and polyunsaturated fats is more effective in preventing coronary heart disease in women than reducing overall fat intake.2
The American Heart Association (AHA) recommends that 15 to 30 per cent of calories in the diet come from fat. Of this, a maximum of 10 per cent should come from saturated fats and also no more than 10 per cent from polyunsaturated fatty acids. The AHA also recommends that intake of dietary cholesterol, which is only found in animal foods, should be no more than 300 mg per day. Only saturated fatty acids and dietary cholesterol raise blood cholesterol. Some experts recommend very low fat diets to reduce the risk of, and even actually reverse damage caused by atherosclerosis. One such diet, which is known as the Ornish diet, recommends limiting fat intake to 10 per cent of calories.
The AHA recommends that 50 to 55 per cent, or more, of calories should come from carbohydrates, with the emphasis mainly on complex carbohydrates such as vegetables, beans and grains. Complex carbohydrates are absorbed more slowly into the blood than simple carbohydrates. This avoids the sharp rises and falls in insulin that a diet high in simple sugars can cause. Refined sugar also seems to cause a greater increase in blood fat levels than more complex carbohydrates.
In fat tissue, insulin facilitates the storage of glucose and its conversion to fatty acids, and also slows the breakdown of fatty acids. Thus sharp rises in insulin may contribute to obesity and heart disease, and it seems that blood insulin stores correspond to body fat stores. The longer and more often insulin levels are high the more likely sugars are to be converted to and stored as fat. This increases the risk of obesity and cardiovascular disease. Eating large amounts of foods high in both fat and sugar further increases the risk.
Diets high in animal protein seem to raise the risk of cardiovascular disease while diets high in vegetable proteins lower it.
Vitamins, Minerals and Cardiovascular Disease
Data from many sources, including laboratory experiments, epidemiology, animal studies and some clinical trials suggest that antioxidants may protect against the development of cardiovascular disease. The evidence is strongest for vitamin E and weakest for vitamin C.
Antioxidants may help prevent heart disease in a number of ways. They improve blood cholesterol levels and protect LDL cholesterol from oxidation. Oxidized LDL cholesterol is more likely to block arteries than unoxidized LDL cholesterol. Oxidized LDL cholesterol can also impair the action of nitric oxide, a chemical secreted by the blood vessel wall which dilates arteries. Levels of beneficial HDL cholesterol may be lowered by free radical activity. Antioxidants also help prevent the aggregation of blood platelets which can stick to blood vessel walls and cause blockages.
It is not yet clear what dose or in what combination, antioxidants provide the best protection. At the very least, it is important to consume the recommended dietary allowances for all antioxidants, especially from food which contains many other heart protective chemicals.
Many large population studies show that the risk of heart disease decreases with increasing beta carotene intake. Researchers involved in the Massachusetts Health Care Panel Study examined the links between consumption of carotene-containing fruits and vegetables, and death from cardiovascular disease among 1299 elderly people. The results of the study, which were published in the Annals of Epidemiology in 1995 showed that during the follow-up period of almost five years, there were 161 deaths from cardiovascular disease. The risk of death in the group who ate the most carotene-containing foods was almost half that of those people whose carotene consumption was low.3
Results from the EURAMIC study suggest that antioxidants protect heart attacks. Researchers studied people from ten European countries and analyzed for levels of carotenes in those who had suffered heart attacks and those who had not. They found protective effects of alpha carotene, beta carotene, and lycopene. Lycopene was particularly protective, with those in the highest intake group having around half the risk of heart attack of those in the lowest intake group.4
In a 1997 study, researchers in Italy investigated the relationship between nonfatal heart attacks and dietary intake of beta carotene. The study involved 433 heart attack patients and 869 women without cardiovascular disease. The results showed that women with high beta carotene intakes had around half the risk of heart attack of those with low intakes.5 The relationship between intake of dietary antioxidants and risk of stroke was investigated as part of the Chicago Western Electric Study. The researchers found a moderately reduced risk in those with high beta carotene intakes.6
Beta carotene supplements have been used in cancer and cardiovascular disease prevention trials including the Finnish Alpha Tocopherol Beta Carotene Cancer (ATBC) Prevention Study, the US Carotene and Retinol Efficacy Trial (CARET) and the US Physicians Health Study. In 1996 these studies reported results which received wide publicity. The ATBC Prevention group studied 29,000 men who smoked and drank alcohol. The results showed an 18 per cent increase in lung cancer deaths and an 11 per cent increase in ischemic heart disease deaths in men who took daily supplements of 20 mg beta carotene.7 The CARET study was stopped 21 months early. This study was examining the effect of beta carotene (30 mg daily) and retinol (7500 mcg RE daily) supplementation on the prevention of cancer and heart disease in over 18,000 smokers and people who had been exposed to asbestos. The trial was stopped when the results showed a 28 per cent increased risk of lung cancer, a 26 per cent increase in the risk of death from cardiovascular disease and a 17 per cent increase in overall deaths in the group receiving the supplements.8
It seems likely that smoking and alcohol consumption contribute to the adverse effects of beta carotene supplements. The CARET results showed greater risk in current smokers than former smokers and also in those who drank alcohol. Recent laboratory research suggests that vitamin C protects against the harmful effects of beta carotene in smokers. Smokers tend to have low levels of vitamin C and this may allow a build-up of a harmful form of beta carotene called the carotene free radical which is formed when beta carotene acts to regenerate vitamin E. These results suggest that in smokers, dietary vitamin C supplementation should accompany beta carotene supplementation.9
Vitamin C
Low vitamin C intake is linked to an increased risk of cardiovascular disease. As well as exerting beneficial effects on cholesterol levels, vitamin C also increases the production of prostacyclin, a prostaglandin which decreases the clumping of blood platelets and dilates blood vessels, therefore reducing the risk of heart disease, atherosclerosis and stroke.
In a study begun in 1981, USDA researchers assessed the health and nutrition status of 747 elderly people aged 60 years and over. Particular attention was paid to the foods the participants usually ate their blood levels of the antioxidant vitamins C, E and beta carotene. The researchers following up the subjects from nine to 12 years later found that among people who ate lots of dark green and orange vegetables, there were fewer deaths from heart disease and other causes. The results showed that a daily intake of more than 400 mg and higher blood levels of vitamin C were linked to reduced risk of death from heart disease.10
In a study published in the British Medical Journal in 1995, UK researchers assessed the links between dietary intake and blood levels of vitamin C, and death from stroke and coronary heart disease in people aged 65 and over. The study involved 730 men and women who were followed up for a 20- year period. The results showed that those with the highest intakes had around half the risk of death from stroke when compared to those with the lowest intakes. However, in this study, no link was found between vitamin C status and risk of death from coronary heart disease.11
Low vitamin C levels are also associated with an increased risk of heart attack. In a 1997 study, Finnish researchers examined this link in 1605 men aged between 42 and 60 who were free from heart disease when they entered the study. During the follow-up period there were 70 heart attacks. The results showed that men with vitamin C deficiency were three-and-a-half times more likely to have a heart attack than those who were not deficient.12 However, not all studies have shown protective effects of vitamin C. These include the large Nurses and Health Professionals Studies.13,14
Researchers from Cambridge University in the UK examined the relationship between blood levels of vitamin C status and angina in women aged from 45 to 74. Forty-two women with previously undiagnosed angina were compared with 877 women with no disease. Those with higher vitamin C levels had a 66 per cent reduced risk of angina.15 The same researchers examined the link between blood levels of vitamin C and blood fat levels. Their results showed that a high intake of vitamin C from food raises beneficial HDL cholesterol and lowers serum triglyceride.16
Vitamin C supplements may help protect against the development of cardiovascular disease. The results of a 1996 study showed that those taking vitamin E supplements had a 47 per cent lower risk of death from heart disease and those taking both vitamin C and vitamin E had a 53 per cent reduced risk.17
High fat meals cause damage to artery linings, which may contribute to the development of atherosclerosis. Research suggests that taking the antioxidant vitamins C and E before a meal may help to prevent this damage.18 Vitamin C may also improve artery function in those with coronary artery disease19, high cholesterol levels20 and chronic heart failure.21 When blood is re-supplied to an organ from which it was previously cut off, oxidative damage can occur. This has been found in many types of surgery; for example, in heart bypass operations. Vitamin C has been shown to protect against this reperfusion injury.22
Vitamin C also seems to protect against smoking-related damage, possibly by decreasing the smoking-related build-up of atherosclerotic plaque and by improving artery function.23
Vitamin E
High intakes of vitamin E may reduce the risk of heart disease. Some studies have only shown benefit from the amount of vitamin E that can be obtained in the diet, whereas others suggest that the amount of vitamin E needed to show protective effects is considerably more than a typical diet provides.
Results from the Iowa Women's Health Study suggest a link between low vitamin E intake and heart disease. Researchers studied 34,486 postmenopausal women with no cardiovascular disease who in early 1986 completed a questionnaire that assessed, among other factors, their intake of vitamins A, E, and C from food sources and supplements. During seven years of follow-up, 242 women died of coronary heart disease. The results showed that high vitamin E consumption reduced the risk of death from coronary heart disease. This association was particularly striking in the subgroup of 21,809 women who did not consume vitamin supplements.24
Similar results have been seen in men. Harvard School of Public Health researchers have assessed the links between diet and heart disease in 39,910 US male health professionals aged between 40 to 75 years of age. Participants responded to a questionnaire in 1986 and were then followed up for four years, during which time there were 667 cases of coronary disease. The results showed a lower risk of disease among men with higher intakes of vitamin E. Men consuming more than 40 mg (60 IU) per day had a 36 per cent lower risk than those consuming less than 5 mg (7.5 IU) per day. Men who took at least 67 mg (100 IU) per day for at least two years had a 37 per cent lower risk than those who did not take supplements.25
Vitamin E appears to play a part in decreasing the risk of angina. The results of a 1996 study done in Japan suggest that low vitamin E levels increase the risk of a variant angina, a form of the disease caused by coronary artery spasm.26 Results of the Finnish ATBC Prevention Study found a slightly reduced risk in those taking vitamin E supplements.27
Results from the Nurses Health Study provide evidence for the protective effects of vitamin E supplements. Researchers assessed the links between vitamin E and heart disease in 87,245 female nurses aged from 34 to 59. During the follow-up period of eight years, there were 552 cases of major coronary disease (437 nonfatal heart attacks and 115 deaths due to coronary disease). The results showed that women with the highest vitamin E intakes had 34 per cent less risk of major coronary disease compared to those with the lowest intakes. Most of the reduction in risk was attributable to vitamin E consumed as supplements, a finding which conflicts with some other studies which only show benefit from high dietary intakes. Women who took vitamin E supplements for short periods had little apparent benefit, but those who took them for more than two years had an even lower risk of disease.28
Results from a British study known as the Cambridge Heart Antioxidant Study (CHAOS) which were published in The Lancet in 1996 provide further evidence of a link between vitamin E supplements and reduction in heart disease risk. In this double-blind, placebo-controlled study, 2002 patients with coronary atherosclerosis were enrolled and followed up for 510 days. 546 patients were given 536 mg (800 IU) daily; 589 patients were given 268 mg (400 IU) per day; and 967 received identical placebo capsules. The results showed that those who received vitamin E supplements had a 75 per cent reduction in the risk of fatal heart attacks. However, when nonfatal events were included, there did not appear to be any benefit from the vitamin E supplements.29
B vitamins
Marginal thiamin deficiency may contribute to heart disease as those with heart disease have been found to have lower than normal levels of thiamin in their heart muscle.
Large doses of the nicotinic acid form of niacin are used to lower harmful LDL blood cholesterol and triglyceride levels, and raise levels of beneficial HDL cholesterol. Niacin also favorably influences other lipid levels including lipoprotein (a). Doses used range from 1500 to 2500 mg. The increase of HDL cholesterol seems to occur at a lower dose (1500 mg per day) than the reduction of LDL cholesterol. In general, it is usual to start taking lower doses (around 50 to 100 mg) and then gradually increase to the higher doses over a period of two to three weeks.
Researchers involved in a 1997 study done in Minneapolis compared blood lipid levels in 244 patients treated with niacin and 160 treated with lovastatin, a widely used cholesterol-lowering drug. The results showed that both lovastatin and niacin effectively reduced LDL cholesterol levels with a greater drop seen in those taking lovastatin. Niacin use was associated with a 16.3 per cent improvement in HDL cholesterol, while HDL cholesterol levels in the lovastatin group improved 1.5 per cent. The improvement in triglyceride levels was also much greater in the niacin group.35
Nicotinic acid can also enhance the effects of other cholesterol-lowering medications. This may mean that the doses of these drugs can be reduced, thus lessening the possibility of undesirable side effects. In a recent US study researchers found that combination therapy with niacin and low dose lovastatin was as effective as high dose lovastatin.36
Nicotinic acid has also been shown to have favorable effects on the blood clotting system which can reduce the build-up of atherosclerotic plaque.37 It has also been used to treat peripheral vascular disease and circulatory disorders such as Raynaud's disease, as it dilates blood vessels thereby increasing blood flow to certain areas of the body.
Vitamin B6
Vitamin B6 deficiency seems to increase the risk of developing heart disease, most likely because of increased homocysteine levels. In a study published in 1998, researchers involved in a study done in several centers in Europe compared 750 patients with vascular disease and 800 control subjects of the same ages and sex. They measured blood levels of homocysteine, folate, vitamin B12, and vitamin B6. The results showed that those with high blood homocysteine concentrations had a high risk of vascular disease. In addition, low concentrations of folate and vitamin B6 were also associated with increased risk. In this study, the relationship between vitamin B6 and atherosclerosis did not appear to be solely due to increased homocysteine levels, suggesting that vitamin B6 may have other important roles in heart disease prevention.38
Researchers involved in the Framingham Heart Study analyzed blood samples from the study participants to assess levels of homocysteine and the relationship between B vitamins and carotid artery narrowing, which increases the risk of heart attack. The results showed that low intakes of folate and vitamin B6 were associated with high homocysteine levels.39
Intake of folate and vitamin B6 above the current recommended dietary allowance seems to be important in the prevention of coronary heart disease among women. Researchers from the Harvard School of Public Health investigated the links between intakes of folate and vitamin B6 and the incidence of heart attacks in 80,082 women taking part in the Nurses Health Study. The women had no previous history of cardiovascular disease, cancer, high cholesterol levels or diabetes when they entered the study. During the 14 years of follow-up, there were 658 nonfatal heart attacks and 281 fatal ones. The results showed that those with the highest intakes of vitamin B6 had just over 30 per cent less risk of heart attack than those in the low intake group. Women in the group with the highest intakes of both folate and vitamin B6 had just less than half the risk of women in the lowest intake group. Risk of coronary heart disease was reduced among women who regularly used multiple vitamins, the major source of folate and vitamin B6.40
In a study published in 1998, Irish researchers screened a group of clinically healthy working men aged 30 to 49 years and selected 132 with mildly raised homocysteine concentrations. They then assessed the effects of eight weeks of supplementation with B group vitamins and antioxidant vitamins on homocysteine concentrations. The men were randomly assigned to one of four groups: supplementation with B group vitamins alone (1 mg folic acid, 7.2 mg pyridoxine, and 0.02 mg vitamin B12); antioxidant vitamins alone; B-group vitamins with antioxidant vitamins; or placebo. The results showed significant decreases in both groups receiving B group vitamins either with or without antioxidants. The effect of the B group vitamins alone was a reduction in homocysteine concentrations of almost 30 per cent.41
Vitamin B6 may also exert beneficial effects on the cardiovascular system by protecting against the aggregation of blood platelets. This prolongs clotting time and helps to reduce atherosclerotic plaque build-up.42 Vitamin B6 has also been shown to lower blood pressure and blood cholesterol levels. In a Swedish study published in 1990, researchers assessed the effect of 120 mg a day of vitamin B6 on seventeen 88 year-old men with low vitamin B6 levels. After supplementation for eight weeks, the average plasma total cholesterol and LDL cholesterol concentrations were decreased by 10 per cent and 17 per cent respectively.43
Folic acid
Diets high in folic acid seem to reduce the risk of heart disease. As with vitamin B6, this is likely to be due to the relationship with homocysteine levels. In a study published in 1998, researchers at the Cleveland Clinic conducted a study to investigate the relationships between homocysteine, B vitamins, and vascular diseases. The study involved 750 patients with documented vascular disease and 800 control patients matched for age and sex. The results showed that those in the lowest 10 per cent of folate intakes had an increased risk of disease.44
A 1996 Canadian study of the relationship between fatal coronary heart disease and folic acid levels in 5000 men and women found that the risk of coronary heart disease increased as folic acid levels decreased. Those in the lowest intake group were 69 per cent more likely to die of heart disease than those with the highest intakes.45
Low blood folic acid levels also seem to increase heart attack risk in young women. In a 1997 study, researchers at the University of Washington measured the homocysteine, folic acid and vitamin B12 levels in 79 heart attack survivors under 45 and compared these with levels in 386 healthy control subjects. Those with the highest homocysteine levels had 2.3 times the risk of heart attack compared to those with the lowest levels. Those with the highest levels of folic acid had around half the risk of heart attack compared to those with the lowest levels.46
Several studies have examined the homocysteine-lowering effects of folate supplements. In a 1998 paper, researchers analyzed the results of randomized controlled trials that assessed the effects of folic acid-based supplements on blood homocysteine concentrations. The data included that from 1114 people in 12 trials. They found that 0.5 to 5 mg folic acid daily reduced blood homocysteine concentrations by 25 per cent.47 Those with the highest homocysteine levels may respond best to increases in folic acid intake; and above a certain level of intake, increasing folic acid may not affect homocysteine levels. In a 1997 Irish study, researchers assessed the effects of various doses of supplements on homocysteine levels. Of the three folic acid doses, 200 mcg appeared to be as effective as 400 mcg, while 100 did not lower levels sufficiently.48
Vitamin B12
Vitamin B12 may also be important in maintaining normal levels of homocysteine.49
Vitamin D
Low vitamin D levels may also increase the risk of atherosclerosis. Research suggests that a low level of vitamin D increases the risk of calcium build-up in atherosclerotic plaques, and that higher levels reduce the risk of build-up. Researchers at UCLA School of Medicine measured the vitamin D levels in the blood of 173 men and women at risk of heart disease and also measured the build-up of calcium in coronary arteries (a common finding in coronary artery disease). The results suggest that calcium may regulate calcium deposition in the arteries as well as in the bone.50
Minerals and Cardiovascular Disease
Although there is no evidence for a direct cause and effect relationship between mineral and trace element status and atherosclerosis in humans, many elements exert a strong influence on individual risk factors for cardiovascular disease, such as disorders of blood fats, blood pressure and blood clotting. Epidemiological studies have shown that high intakes of minerals such as sodium, magnesium, calcium, chromium, copper, zinc, and iodine lead to a reduced risk of cardiovascular disease. The local environment, which influences the mineral content of food and dietary practices, can result in mineral and trace element imbalances. Deficiencies of chromium, iron, copper, zinc, selenium, and iodine are relatively common. Detection and correction of such imbalances in people may diminish risk factors and reduce the incidence of atherosclerotic heart disease.
Calcium plays an important role in heart health. It is essential for heart muscle contraction, nerve impulse conduction, blood pressure regulation, and is involved in the control of blood cholesterol levels. Increasing calcium may normalize heart rhythm in arrhythmia sufferers. Calcium supplements can be useful in congestive heart failure as they increase the contractility of heart muscle. Calcium salts are used intravenously to treat heart attack associated with high potassium and magnesium levels and low calcium levels.
Chromium deficiency may play a role in heart disease. On a population level, decreased chromium levels correlate with increased prevalence of heart disease. Recent studies have demonstrated that plasma chromium levels in patients with coronary artery disease are very much lower than in normal subjects. Chromium deficiency leads to impaired lipid and glucose metabolism and results in high cholesterol levels.
In a study published in 1996, researchers assessed the effects of daily supplements of 200 mcg of chromium and nicotinic acid on blood glucose and lipids, including total cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides. The patients were 14 healthy adults and five adults with Type II diabetes mellitus. The results showed lowered total and LDL cholesterol, triglycerides, and glucose concentrations in patients with Type II diabetes.51
A deficiency of copper may contribute to heart disease. It may lead to a drop in beneficial HDL cholesterol and an increase in harmful LDL cholesterol. In animals, copper intake has also been associated with weakening of heart connective tissue and rupture of heart muscle. However, high copper levels may also be a risk factor for heart disease. The ratio of zinc to copper may be important in the regulation of blood cholesterol.
Copper supplements have been shown to have beneficial effects on the oxidation of blood fats. A 1997 study done over four weeks at Ohio State University found that 2 mg per day of copper increased the time taken for LDL cholesterol to become oxidized.52 This helps to reduce the damage these fats do to arteries, and limits the build-up of atherosclerotic plaque.
Iron deficiency can adversely affect the heart, leading to abnormal heartbeat and heart function. However, the evidence from many scientific studies suggests that high iron levels (above 200 mcg per liter blood ferritin) may lead to an increase in the risk of cardiovascular disease. The increased risk may be due to oxidative damage to the heart and blood vessels, and increased oxidation of LDL cholesterol.
A study published in 1998 in the American Journal of Epidemiology suggests that men and women, particularly those over 60, are at increased risk of heart disease if they have high levels of iron in their diets. The study, which was conducted in Greece, involved 329 patients with heart disease and 570 people of similar age who were admitted to hospital with minor conditions believed to be unrelated to diet. Results showed that for every 50 mg increase in iron intake per month, men over 60 were 1.47 times more likely to have heart disease than their peers. In women over 60, the risk was even higher; with a 3.61-fold risk for every 50 mg increase.53
Another study published in 1998 in the journal Circulation suggests that men with high levels of stored iron in the body have an increased risk of heart attack. The study, which was done in Finland, involved 99 men who had had at least one heart attack and 99 healthy men matched for background and age. The results showed that those men with the highest iron levels had almost three times the risk of heart attack when compared to those with the lowest levels.54 Further research is needed to confirm this link and to establish whether this applies to women whose blood ferritin levels are typically much lower (20 to 120 mcg per liter). Some experts believe that women are protected from heart disease until after menopause due to iron losses during menstruation.
However, a National Institute of Aging study suggests that low iron levels are linked to an increased likelihood of death in elderly people. Researchers looked at the iron status of nearly 4000 men and women aged 71 and over. Results of the five-year study showed that low iron levels increased the risk of total and coronary heart disease deaths. Those with higher iron levels had decreased risk. Men with the highest iron levels had only 20 per cent of the risk of dying of heart disease of those with the lowest levels. Women with the highest levels were about half as likely to die of heart disease compared to those with the lowest levels.55
High magnesium intake seems to protect against several types of cardiovascular disease, including atherosclerosis, heart attack, angina, ischemic heart disease and cardiac arrhythmias. Magnesium deficiency may increase the risk of cardiovascular disease in several ways. Chronic magnesium deficiency in animals has been shown to result in microscopic changes in the heart arteries and the development of atherosclerosis. Deficiency also leads to changes in the heart muscle itself, including cell degeneration, fibrosis, necrosis and calcification. Blood fat levels are also affected by magnesium dietary intake. Cholesterol may be more susceptible to oxidative damage when magnesium levels are low.
Studies show that death rates from coronary heart disease are higher in areas where the water is low in magnesium. In a 1996 study, Swedish researchers investigated these links in 17 municipalities in the southern part of the country which had differing water magnesium concentrations. The study included 854 men who had died of heart attacks between the ages of 50 and 69, and 989 men of the same age in the same area who had died from cancer during the same time period. The results showed that men living in high magnesium water areas had a 35 per cent lower chance of death from heart attack than those who drank low magnesium water.56
Results from the Atherosclerosis Risk in Communities (ARIC) Study support the association between low serum and dietary magnesium and various types of cardiovascular disease including high blood pressure. A total of 15,248 people took part, male and female, black and white, aged 45 to 64 years. The results showed that serum magnesium levels were significantly lower in participants with cardiovascular disease, high blood pressure, and diabetes than in those free of these diseases. Low dietary intake was linked to lower beneficial HDL cholesterol levels and thicker carotid artery walls, both of which increase the risk of cardiovascular disease.57
Magnesium deficiency is also linked to variant angina, a disorder in which coronary heart vessels go into spasm.58 A 1996 Japanese study found that men with lower magnesium levels had more frequent and severe angina attacks.59 Magnesium-deficient heart muscle is more vulnerable to lack of oxygen.
Magnesium deficiency also contributes to cardiac arrhythmias, possibly because magnesium is responsible for maintaining potassium concentrations inside muscle cells. Potassium plays a role in heart muscle contraction. Magnesium deficiency has been implicated in mitral valve prolapse, a disorder in which the mitral valve in the heart fails to properly close off the heart chambers from each other during contraction. As many as 85 per cent of sufferers may have chronic magnesium deficiency.
Low magnesium levels have been found in the blood and cardiac muscle of heart attack victims, and several small studies have shown that magnesium sulfate injections can reduce death rates in heart attack patients, both in the short term and for longer periods.60 It may act by improving energy production, inhibiting platelet aggregation, reducing vascular resistance, promoting clot breakdown, dilating blood vessels and improving the function of heart muscle. It also protects the damaged heart muscle against calcium overload and reduces free radical damage.
However, two recently published studies showed different results, although similar doses of magnesium were used. The LIMIT-2-study was a double-blind, placebo-controlled investigation of over 2300 patients with suspected heart attack. Magnesium infusion reduced 28-day death risk by 24 per cent.61 The ISIS-4-study on over 50,000 patients with suspected heart attack did not show any positive effect of magnesium on death rate.62
Magnesium supplements are often used to treat angina, both that caused by atherosclerosis and variant angina caused by coronary artery spasm. In a 1997 study UK researchers assessed the effects of a 24-hour infusion of magnesium in patients with unstable angina. Thirty-one patients received magnesium sulfate and 31 placebo. After treatment, there were fewer ischemic episodes in the magnesium group and duration of ischemia in the placebo group was longer than that in the magnesium group.63
Magnesium supplements have also been used to treat cardiomyopathy, a weakening of heart muscle which leads to reduced efficiency of blood circulation and congestive heart failure. Sufferers of intermittent claudication, a painful condition caused by reduced blood flow to the legs, often have low magnesium levels and may be helped by supplements. Magnesium supplements have been successfully used to treat mitral valve prolapse.64 Magnesium supplements have been shown to reduce cholesterol and triglyceride levels.
High potassium intake is associated with protection from cardiovascular disease and several studies have shown that increasing potassium intake can lower blood pressure. Potassium may protect against cardiovascular diseases in a number of ways: by reducing free radical formation; proliferation of vascular smooth muscle cells; platelet aggregation; and blood clotting.65 Potassium supplements are used to treat heart arrhythmias.
High sodium intake is linked to an increased risk of high blood pressure and other cardiovascular diseases. The American Heart Association recommends that the daily sodium intake for healthy American adults should not be more than 2.4 g per day. This is about one teaspoon of salt.
Low selenium levels are linked to an increased risk of heart disease. Severe deficiency leads to weakened and damaged heart muscle and a type of congestive heart failure known as Keshan disease. As part of glutathione peroxidase, selenium takes part in the reduction of hydrogen peroxides and lipid peroxides. The concentration of these peroxides, in turn, affects platelet aggregation. Blood platelets of selenium-deficient people show increased aggregation, which selenium administration inhibits. Thus long-term supplementation with low doses of selenium could have a beneficial effect on the prevention of both thrombosis and coronary heart disease in people who are selenium-deficient.30
Dutch researchers studying the association between selenium status and the risk of heart attack, compared plasma, red blood cell, and toenail selenium levels and the activity of red blood cell glutathione peroxidase among 84 heart attack patients and 84 healthy people. They found lower selenium levels in all the heart attack patients. Because the toenail selenium level reflects blood levels up to one year before sampling, the results suggest that low selenium levels were present before the heart attacks, and may have played a role in their cause.31
However, results from the Physicians Health Study published in 1995 do not suggest a link between selenium levels and heart attack risk. Researchers analyzed blood selenium levels in 251 subjects who had heart attacks and an equal number of healthy people, matched by age and smoking status. The results did not show significant differences.32
Finnish researchers evaluated the effect of selenium supplementation on 81 patients with heart attacks. Patients received either selenium-rich yeast (100 mcg per day) or placebo in addition to conventional drug therapy for a six- month period. During the follow-up period there were four cardiac deaths in the placebo group but none in the selenium group. There were two nonfatal heart attacks in the placebo group and one nonfatal attack in the selenium group.33 A small 1997 German study showed that patients who were given selenium supplements after heart attacks showed greater improvements in heart function than patients not given supplements.34
Low blood zinc levels may be associated with an increased risk of cardiovascular disease. The results of a recent study done over a period of ten years in Finland, which involved 230 men dying from cardiovascular diseases and 298 controls matched for age, place of residence and smoking found an increased risk of disease in those with low zinc levels.66 This may be due to an imbalance in the copper-to-zinc ratio.
There is evidence that zinc can protect the inner lining of blood vessels from damage thus helping to prevent atherosclerosis. This may be due to its membrane-stabilizing, antioxidant and anti-inflammatory properties.67 Some studies have shown that zinc supplements can reduce free radical damage to blood fats. In a 1996 Italian study, 25 mg zinc sulfate in 136 elderly people decreased plasma lipid peroxides.68 This can help to reduce the risk of cardiovascular disease.
Other Nutrients
Essential Fatty Acids
Some studies have shown that those who regularly eat fish have lower rates of heart disease. Fish are rich in omega-3 fatty acids, which can lower blood levels of triglycerides and LDL cholesterol. Fish oils can also interfere with the ability of blood to clot, which also protects against cardiovascular disease.
There are many population studies demonstrating that people who consume omega-3 fatty acid-rich diets have a reduced risk of heart disease. This was first noticed in countries such as Greenland and Japan where fish consumption is particularly high. Studies in other countries have found similar effects. In a study reported in the New England Journal of Medicine, researchers in Holland investigated the relationship between fish consumption and coronary heart disease in a group of men in the town of Zutphen. Information about the fish consumption of 852 middle-aged men without coronary heart disease was collected in 1960. During 20 years of follow-up, 78 men died from coronary heart disease. The results showed that compared to those who did not eat fish, death from coronary heart disease was more than 50 per cent lower in those who ate at least 30 g of fish per day.69 However, not all studies have shown a reduced risk in those who regularly eat fish.
In a study reported in 1989, researchers examined the effects of dietary changes in the prevention of further heart attacks in 2033 men who had recovered from one attack. Some of the men were given various pieces of dietary advice, one of which was to increase the consumption of fatty fish to around two or three portions per week. Those advised to do this had a 29 per cent reduction in death from all causes and a 33 per cent reduction in death from heart attack compared with those who were not advised to eat fish.70 These beneficial effects may be due to the anti-arrhythmic effects of omega-3 fatty acids.
Researchers involved in the US Physicians Health Study investigated the links between fish consumption and the risk of sudden death from heart attack in 20,551 US male physicians aged from 40 to 84. The follow-up period was 11 years, and in that time there were 133 sudden deaths. The results showed that men who ate fish at least once per week had around half the risk of sudden cardiac death when compared with men who consumed fish less than once a month. Neither dietary fish consumption nor omega-3 fatty acid intake was associated with a reduced risk of total heart attack, nonsudden cardiac death, or total cardiovascular mortality. However, fish consumption was associated with a significantly reduced risk of death from all causes.71
In a 1995 study, researchers at the University of Washington examined the links between risk of heart attack and the consumption of fatty acids from seafood, and assessed both directly and indirectly through examination of blood samples. The study involved 334 patients with primary cardiac arrest and 493 population-based control cases, matched for age and sex. The results showed that an intake of 5.5 g of omega-3 fatty acids (equivalent to one fish-containing meal a week) reduced the risk of heart attack by 50 per cent. Their results also showed a correlation between higher red blood cell levels of omega-3 fatty acids and reduction in risk of heart attack. Those with the highest levels had a 70 per cent reduction in risk compared to those with the lowest levels.72
Omega-3 fatty acid supplements have been used to treat and prevent various types of cardiovascular disease. Supplements have been shown to have beneficial effects on cholesterol and triglyceride levels. In a 1994 study, researchers assessed the effects of fish oil supplements on 350 men and women aged from 30 to 54 years who were enrolled in a hypertension prevention trial. Once a day for six months, the participants received either a placebo or 6 g of purified fish oil, which supplied 3 g of omega-3 fatty acids. The results showed that the fish oil increased HDL cholesterol levels significantly. The effect was more marked in the women.73
Supplements have also been shown to affect blood clotting through effects on platelets and to lead to a reduction in production of prostaglandins and other substances that damage artery walls.74 Other studies have shown that omega-3 fatty acids reduce the build-up of white blood cells in atherosclerotic plaque. A 1997 Australian study showed that flaxseed oil improved the elasticity of artery walls. This tends to decrease with increasing cardiovascular risk and has also been shown to improve with increasing intake of omega-3 fatty acids from fish.75
Choline helps to lower cholesterol levels as a choline-containing enzyme helps to remove cholesterol from tissues. In a 1995 study, researchers gave lecithin supplements to 32 patients with high cholesterol and triglyceride levels. The dosage used was 3.5 g three times daily before meals. After 30 days of treatment, total cholesterol and triglycerides levels decreased significantly and beneficial HDL cholesterol levels rose.76 Choline has also been used to lower homocysteine concentrations.
Coenzyme Q10
Increasing scientific evidence suggests that coenzyme Q10 is a safe and effective therapy for a wide range of cardiovascular diseases such as congestive heart failure, cardiomyopathy, high blood pressure, mitral valve prolapse and angina. It has also been used to treat patients undergoing coronary artery bypass surgery. Coenzyme Q10 appears to exert its beneficial effects both by improving energy production and by acting as an antioxidant.
Coenzyme Q10 may help prevent atherosclerosis as it can protect against oxidative damage to fats. In a 1993 Japanese study, researchers measured levels of coenzyme Q10 and also levels of various types of cholesterol and other blood fats in 378 people. These included 249 people with no coronary artery disease, 29 patients with the disease who were receiving pravastatin, (a cholesterol-lowering drug) and 104 patients with the disease who were not receiving pravastatin. In the patient groups, the plasma total cholesterol and LDL cholesterol levels were higher and the plasma coenzyme Q10 level lower than in those with no disease. The results showed that coenzyme Q10 levels, either alone or when expressed in relation to LDL levels, were significantly lower in the patient groups compared with those with no disease. They concluded that coenzyme Q10 therapy would be beneficial in patients with atherosclerosis.77
In a study published in 1994, researchers at the University of Texas looked at the usefulness of long-term coenzyme Q10 therapy in clinical cardiology. Over an eight-year period, they treated 424 patients with various forms of cardiovascular disease by adding coenzyme Q10, in amounts ranging from 75 to 600 mg/day to their treatment programs. Patients were divided into six diagnostic categories including ischemic cardiomyopathy, dilated cardiomyopathy, primary diastolic dysfunction, hypertension, mitral valve prolapse and valvular heart disease.
The patients were followed for an average of 17.8 months. The researchers evaluated clinical response according to the New York Heart Association (NYHA) functional scale and found significant improvements in all the patients. Out of 424 patients, 58 per cent improved by one NYHA class, 28 per cent by two classes and 1.2 per cent by three classes. Statistically significant improvements in heart muscle function were shown using a variety of laboratory tests. Before treatment with coenzyme Q10, most patients were taking from one to five cardiac medications and during the study, overall medication requirements dropped considerably with 43 per cent of patients stopping between one and three drugs. Only 6 per cent of the patients required the addition of one drug. No apparent side effects from coenzyme Q10 treatment were noted other than a single case of transient nausea. The researchers concluded that coenzyme Q10 is a safe and effective treatment for a broad range of cardiovascular diseases, often in combination with other medications, as it produces improvements in a variety of symptoms and reduces medication needs.78
Coenzyme Q10 has also been used during heart surgery and to treat heart failure, cardiomyopathy and angina (See page 355 for more information.)
Carnitine can be used to treat several types of cardiovascular disease including cardiomyopathy, angina, heart attack and arrhythmias. It can also be used to lower blood fat levels, aid in weight loss, and improve muscle strength in some cases of weakness.
Herbal Medicine and Cardiovascular Disease
There are many herbs used in the treatment of cardiovascular conditions. These include, garlic (Allium sativum), onions (Allium cepa), ginger (Zingiber officinale), gugulipid (Commiphora mukul), cayenne (Capsicum annuum), ginkgo (Ginkgo biloba), yarrow (Achillea millefolium), linden blossom (Tilia europea) and cramp bark (Viburnum opulus).
1 Rimm EB; Ascherio A; Giovannucci E; Spiegelman D; Stampfer MJ; Willett WC. Vegetable, fruit, and cereal fiber intake and risk of coronary heart disease among men. JAMA, 1996 Feb, 275:6, 447-51
2 Hu FB; Stampfer MJ; Manson JE; Rimm E; Colditz GA; Rosner BA; Hennekens CH; Willett WC Dietary fat intake and the risk of coronary heart disease in women. N Engl J Med, 1997 Nov, 337:21, 1491-9
3 Gaziano JM; Manson JE; Branch LG; Colditz GA; Willett WC; Buring JE. A prospective study of consumption of carotenoids in fruits and vegetables and decreased cardiovascular mortality in the elderly. Ann Epidemiol, 1995 Jul, 5:4, 255-60
4 Kohlmeier L et al; Lycopene and myocardial infarction risk in the EURAMIC Study. Am J Epidemiol, 1997 Oct, 146:8, 618-26
5 Tavani A; Negri E; DAvanzo B; La Vecchia C. Beta-carotene intake and risk of nonfatal acute myocardial infarction in women. Eur J Epidemiol, 1997 Sep, 13:6, 631-7
6 Daviglus ML; Orencia AJ; Dyer AR; Liu K; Morris DK; Persky V; Chavez N; Goldberg J; Drum M; Shekelle RB; Stamler J Dietary vitamin C, beta-carotene and 30-year risk of stroke: results from the Western Electric Study. Neuroepidemiology, 1997, 16:2, 69-77
7 Albanes D et al; Alpha-Tocopherol and beta-carotene supplements and lung cancer incidence in the alpha-tocopherol, beta-carotene cancer prevention study: effects of base-line characteristics and study compliance J Natl Cancer Inst, 1996 Nov, 88:21, 1560-70
8 Omenn G et al. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med. 1996;334: 1150-5
9 Journal of the American Chemical Society 1997;119:621-622
10 Sahyoun NR; Jacques PF; Russell RM Carotenoids, vitamins C and E, and mortality in an elderly population. Am J Epidemiol, 1996 Sep, 144:5, 501-11
11 Gale CR; Martyn CN; Winter PD; Cooper C Vitamin C and risk of death from stroke and coronary heart disease in cohort of elderly people. BMJ, 1995 Jun, 310:6994, 1563-6
12 Nyyssönen K; Parviainen MT; Salonen R; Tuomilehto J; Salonen JT. Vitamin C deficiency and risk of myocardial infarction: prospective population study of men from eastern Finland. BMJ, 1997 Mar, 314:7081, 634-8
13 Rimm EB; Stampfer MJ; Ascherio A; Giovannucci E; Colditz GA; Willett WC Vitamin E consumption and the risk of coronary heart disease in men. N Engl J Med, 1993 May 20, 328:20, 1450-6
14 Stampfer MJ; Hennekens CH; Manson JE; Colditz GA; Rosner B; Willett WC Vitamin E consumption and the risk of coronary disease in women. N Engl J Med, 1993 May 20, 328:20, 1444-9
15 Ness AR; Khaw KT; Bingham S; Day NE Vitamin C status and undiagnosed angina. J Cardiovasc Risk, 1996 Aug, 3:4, 373-7
16 Ness AR; Khaw KT; Bingham S; Day NE Vitamin C status and serum lipids. Eur J Clin Nutr, 1996 Nov, 50:11, 724-9
17 Losonczy KG; Harris TB; Havlik RJ Vitamin E and vitamin C supplement use and risk of all-cause and coronary heart disease mortality in older persons: the Established Populations for Epidemiologic Studies of the Elderly. Am J Clin Nutr, 1996 Aug, 64:2, 190-6
18 Plotnick GD; Corretti MC; Vogel RA Effect of antioxidant vitamins on the transient impairment of endothelium-dependent brachial artery vasoactivity following a single high-fat meal. JAMA 1997;278:1682-1686
19 Levine GN; Frei B; Koulouris SN; Gerhard MD; Keaney JF Jr; Vita JA Ascorbic acid reverses endothelial vasomotor dysfunction in patients with coronary artery disease. Circulation, 1996 Mar, 93:6, 1107-13
20 Ting HH; Timimi FK; Haley EA; Roddy MA; Ganz P; Creager MA Vitamin C improves endothelium-dependent vasodilation in forearm resistance vessels of humans with hypercholesterolemia. Circulation, 1997 Jun, 95:12, 2617-22
21 Hornig B; Arakawa N; Kohler C; Drexler H Vitamin C improves endothelial function of conduit arteries in patients with chronic heart failure. Circulation, 1998 Feb, 97:4, 363-8
22 Dingchao H; Zhiduan Q; Liye H; Xiaodong F The protective effects of high-dose ascorbic acid on myocardium against reperfusion injury during and after cardiopulmonary bypass. Thorac Cardiovasc Surg, 1994 Oct, 42:5, 276-8
23 Motoyama T; Kawano H; Kugiyama K; Hirashima O; Ohgushi M; Yoshimura M; Ogawa H; Yasue H Endothelium-dependent vasodilation in the brachial artery is impaired in smokers: effect of vitamin C. Am J Physiol, 1997 Oct, 273:4 Pt 2, H1644-50
24 Kushi LH; Fee RM; Sellers TA; Zheng W; Folsom AR. Intake of vitamins A, C, and E and postmenopausal breast cancer. The Iowa Women's Health Study. Am J Epidemiol, 1996 Jul, 144:2, 165-74
25 Rimm EB. Vitamin E consumption and the risk of coronary heart disease in men. N Engl J Med, 328: 20, 1993 May 20, 1450-6
26 Miwa K; Miyagi Y; Igawa A; Nakagawa K; Inoue H Vitamin E deficiency in variant angina. Circulation, 1996 Jul, 94:1, 14-8
27 Rapola JM; Virtamo J; Haukka JK; Heinonen OP; Albanes D; Taylor PR; Huttunen JK Effect of vitamin E and beta carotene on the incidence of angina pectoris. A randomized, double-blind, controlled trial. JAMA, 1996 Mar, 275:9, 693-8
28 Stampfer M et al. Vitamin E consumption and the risk of coronary disease in women. N Engl J Med. 1993;328:1450-1456
29 Stephens N G et al. Randomised controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study (CHAOS). Lancet, 347: 9004, 1996 Mar 23, 781-6
30 5 Vitoux D; Chappuis P; Arnaud J; Bost M; Accominotti M; Roussel AM Selenium, glutathione peroxidase, peroxides and platelet functions. Ann Biol Clin (Paris), 1996, 54:5, 181-7
31 Kok FJ; Hofman A; Witteman JC; de Bruijn AM; Kruyssen DH; de Bruin M; Valkenburg HA. Decreased selenium levels in acute myocardial infarction. JAMA, 1989 Feb 24, 261:8, 1161-4
32 Salvini S; Hennekens CH; Morris JS; Willett WC; Stampfer MJ. Plasma levels of the antioxidant selenium and risk of myocardial infarction among U.S. physicians. Am J Cardiol, 1995 Dec, 76:17, 1218-21
33 Korpela H; Kumpulainen J; Jussila E; Kemilä S; Kääriäinen M; Kääriäinen T; Sotaniemi EA Effect of selenium supplementation after acute myocardial infarction. Res Commun Chem Pathol Pharmacol, 1989 Aug, 65:2, 249-52
34 Thiele R; Wagner D; Gassel M; Winnefeld K; Pleissner J; Pfeifer R Selenium substitution in acute myocardial infarct. Med Klin, 1997 Sep, 92 Suppl 3:, 26-8
35 O'Connor PJ; Rush WA; Trence DL. Relative effectiveness of niacin and lovastatin for treatment of dyslipidemias in a health maintenance organization. J Fam Pract, 1997 May, 44:5, 462-7
36 Gardner SF; Schneider EF; Granberry MC; Carter IR. Combination therapy with low-dose lovastatin and niacin is as effective as higher-dose lovastatin. Pharmacotherapy, 1996 May, 16:3, 419-23
37 Johansson JO; Egberg N; Asplund Carlson A; Carlson LA. Nicotinic acid treatment shifts the fibrinolytic balance favourably and decreases plasma fibrinogen in hypertriglyceridaemic men. J Cardiovasc Risk, 1997 Jun, 4:3, 165-71
38 Robinson K; Arheart K; Refsum H; Brattström L; Boers G; Ueland P; Rubba P; Palma Reis R; Meleady R; Daly L; Witteman J; Graham I. Low circulating folate and vitamin B6 concentrations: risk factors for stroke, peripheral vascular disease, and coronary artery disease. European COMAC Group. Circulation, 1998 Feb, 97:5, 437-43
39 Selhub J; Jacques PF; Bostom AG; DAgostino RB; Wilson PW; Belanger AJ; OLeary DH; Wolf PA; Rush D; Schaefer EJ; Rosenberg IH. Relationship between plasma homocysteine, vitamin status and extracranial carotid-artery stenosis in the Framingham Study population. J Nutr, 1996 Apr, 126:4 Suppl, 1258S-65S
40 Rimm EB; Willett WC; Hu FB; Sampson L; Colditz GA; Manson JE; Hennekens C; Stampfer MJ Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women. JAMA, 1998 Feb, 279:5, 359-64
41 Woodside JV et al. Effect of B-group vitamins and antioxidant vitamins on hyperhomocysteinemia: a double-blind, randomized, factorial-design, controlled trial. Am J Clin Nutr, 1998 May, 67:5, 858-66
42 Sermet A; Aybak M; Ulak G; Güzel C; Denli O Effect of oral pyridoxine hydrochloride supplementation on in vitro platelet sensitivity to different agonists.
43 Brattström L; Stavenow L; Galvard H; Nilsson-Ehle P; Berntorp E; Jerntorp P; Elmståhl S; Pessah-Rasmussen H. Pyridoxine reduces cholesterol and low-density lipoprotein and increases antithrombin III activity in 80-year-old men with low plasma pyridoxal 5-phosphate. Scand J Clin Lab Invest, 1990 Dec, 50:8, 873-7
44 Robinson K; Arheart K; Refsum H; Brattström L; Boers G; Ueland P; Rubba P; Palma Reis R; Meleady R; Daly L; Witteman J; Graham I Low circulating folate and vitamin B6 concentrations: risk factors for stroke, peripheral vascular disease, and coronary artery disease. European COMAC Group. Circulation, 1998 Feb, 97:5, 437-43
45 Morrison HI; Schaubel D; Desmeules M; Wigle DT Serum folate and risk of fatal coronary heart disease. JAMA, 1996 Jun, 275:24, 1893-6
46 Schwartz SM et al. Myocardial infarction in young women in relation to plasma total homocysteine, folate, and a common variant in the methylenetetrahydrofolate reductase gene. Circulation, 1997 Jul, 96:2, 412-7
47 Lowering blood homocysteine with folic acid based supplements: meta-analysis of randomised trials. Homocysteine Lowering Trialists' Collaboration. BMJ, 1998 Mar, 316:7135, 894-8
48 Ward M, McNulty H, McPartlin J, Strain JJ, Weir DG, Scott JM. Plasma homocysteine, a risk factor for cardiovascular disease, is lowered by physiological doses of folic acid. QJM 1997;90:519-24.
49 Chadefaux B; Cooper BA; Gilfix BM; Lue Shing H; Carson W; Gavsie A; Rosenblatt DS. Homocysteine: relationship to serum cobalamin, serum folate, erythrocyte folate, and lobation of neutrophils. Clin Invest Med, 1994 Dec, 17:6, 540-50
50 Watson KE; Abrolat ML; Malone LL; Hoeg JM; Doherty T; Detrano R; Demer LL Active serum vitamin D levels are inversely correlated with coronary calcification. Circulation, 1997 Sep, 96:6, 1755-60
51 Thomas VL; Gropper SS. Effect of chromium nicotinic acid supplementation on selected cardiovascular disease risk factors. Biol Trace Elem Res, 1996 Dec, 55:3, 297-305
52 Jones AA; DiSilvestro RA; Coleman M; Wagner TL Copper supplementation of adult men: effects on blood copper enzyme activities and indicators of cardiovascular disease risk. Metabolism, 1997 Dec, 46:12, 1380-3
53 Tzonou A; Lagiou P; Trichopoulou A; Tsoutsos V; Trichopoulos D. Dietary iron and coronary heart disease risk: a study from Greece. Am J Epidemiol, 1998 Jan, 147:2, 161-6
54 Tuomainen TP; Punnonen K; Nyyssönen K; Salonen JT Association between body iron stores and the risk of acute myocardial infarction in men. Circulation, 1998 Apr, 97:15, 1461-6
55 Corti MC; Guralnik JM; Salive ME; Ferrucci L; Pahor M; Wallace RB; Hennekens CH. Serum iron level, coronary artery disease, and all-cause mortality in older men and women. Am J Cardiol, 1997 Jan, 79:2, 120-7
56 Rubenowitz E; Axelsson G; Rylander R. Magnesium in drinking water and death from acute myocardial infarction. Am J Epidemiol, 1996 Mar, 143:5, 456-62
57 Ma J et al. Associations of serum and dietary magnesium with cardiovascular disease, hypertension, diabetes, insulin, and carotid arterial wall thickness: the ARIC study. Atherosclerosis Risk in Communities. J Clin Epidemiol, 1995 Jul, 48:7, 927-40
58 Goto K; Yasue H; Okumura K; Matsuyama K; Kugiyama K; Miyagi H; Higashi T Magnesium deficiency detected by intravenous loading test in variant angina pectoris. Am J Cardiol, 1990 Mar 15, 65:11, 709-12
59 Satake K; Lee JD; Shimizu H; Ueda T; Nakamura T Relation between severity of magnesium deficiency and frequency of anginal attacks in men with variant angina. J Am Coll Cardiol, 1996 Oct, 28:4, 897-902
60 Rabbani LE; Antman EM The role of magnesium therapy in acute myocardial infarction. Clin Cardiol, 1996 Nov, 19:11, 841-4
61 Woods KL; Fletcher S Long-term outcome after intravenous magnesium sulphate in suspected acute myocardial infarction: the second Leicester Intravenous Magnesium Intervention Trial (LIMIT-2). Lancet, 1994 Apr, 343:8901, 816-9
62 ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group Lancet, 1995 Mar, 345:8951, 669-85
63 26 Redwood SR; Bashir Y; Huang J; Leatham EW; Kaski JC; Camm AJ Effect of magnesium sulphate in patients with unstable angina. A double blind, randomized, placebo-controlled study. Eur Heart J, 1997 Aug, 18:8, 1269-77
64 Lichodziejewska B; K et al. Clinical symptoms of mitral valve prolapse are related to hypomagnesemia and attenuated by magnesium supplementation. Am J Cardiol, 1997 Mar, 79:6, 768-72
65 Young DB, Lin H, McCabe RD. Potassium's cardiovascular protective mechanisms. Am J Physiol 1995 Apr;268(4 Pt 2):R825-R837
66 Reunanen A; Knekt P; Marniemi J; Mäki J; Maatela J; Aromaa A Serum calcium, magnesium, copper and zinc and risk of cardiovascular death. Eur J Clin Nutr, 1996 Jul, 50:7, 431-7
67 Hennig B; Toborek M; Mcclain CJ Antiatherogenic properties of zinc: implications in endothelial cell metabolism. Nutrition, 1996 Oct, 12:10, 711-7
68 Fortes C; Agabiti N; Fano V; Pacifici R; Forastiere F; Virgili F; Zuccaro P; Perruci CA; Ebrahim S Zinc supplementation and plasma lipid peroxides in an elderly population. Eur J Clin Nutr, 1997 Feb, 51:2, 97-101
69 Kromhout D; Bosschieter EB; de Lezenne Coulander C. The inverse relation between fish consumption and 20-year mortality from coronary heart disease. N Engl J Med, 1985 May 9, 312:19, 1205-9
70 Burr ML et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet, 1989 Sep 30, 2:8666, 757-61
71 Albert CM; Hennekens CH; ODonnell CJ; Ajani UA; Carey VJ; Willett WC; Ruskin JN; Manson JE. Fish consumption and risk of sudden cardiac death. JAMA, 1998 Jan, 279:1, 23-8
72 Siscovick DS et al. Dietary intake and cell membrane levels of long-chain n-3 polyunsaturated fatty acids and the risk of primary cardiac arrest. JAMA, 1995 Nov, 274:17, 1363-7
73 Sacks FM et al. Short report: the effect of fish oil on blood pressure and high-density lipoprotein-cholesterol levels in phase I of the Trials of Hypertension Prevention. J Hypertens, 1994 Feb, 12:2, 209-13
74 Mori TA; Beilin LJ; Burke V; Morris J; Ritchie J. Interactions between dietary fat, fish, and fish oils and their effects on platelet function in men at risk of cardiovascular disease. Arterioscler Thromb Vasc Biol, 1997 Feb, 17:2, 279-86
75 Nestel PJ et al. Arterial compliance in obese subjects is improved with dietary plant n-3 fatty acid from flaxseed oil despite increased LDL oxidizability. Arterioscler Thromb Vasc Biol, 1997 Jun, 17:6, 1163-70
76 Wojcicki J et al. Clinical evaluation of lecithin as a lipid-lowering agent. Phytotherapy Res 1995, 9, 597-99
77 Hanaki-Y et al. Coenzyme Q10 and coronary artery disease. Clin Investig. 1993; 71(8 Suppl): S112-5
78 Langsjoen H et al. Usefulness of coenzyme Q10 in clinical cardiology: a long-term study. Mol Aspects Med. 1994; 15 Suppl: s165-75


text:
Strawberry Salad
Be the first to review
READY IN: 2hrs 30mins
Recipe by joyt3595
This fruity gelatin salad is deceptively easy. If someone eats it, he or she will eventually ask for the recipe. Different fruits and gelatins can be used. Enjoy!
See Discussion:
Ingredients Nutrition
- 1 (6 ounce) package strawberry-banana gelatin
- 1 (15 ounce) can crushed pineapple
- 1 (15 ounce) carton fresh strawberries, sliced
- 2 cups boiling water
- 1 (6 ounce) carton sour cream
- 1 (8 ounce) package cream cheese
- 1⁄2 cup sugar
Directions See How It's Made
- Mix gelatin and boiling water.
- Let stand one minute.
- Add pineapple and strawberries and stir well.
- Refrigerate.
- Meanwhile, beat cream cheese and sour cream until fluffy.
- Add sugar and nuts.
- Spread over firm gelatin.
- Refrigerate in 8"x10" glass pan at least one hour.

subset: commoncrawl


text:
I think the Mayor has every right to refuse to talk to whatever paper he wants and not talk to ones he does not want to. The Star agrees with that, but they draw the line when they get cut off from press releases.
Hold on a minute -- why not? What divine automatic right does a newspaper (especially one that continuously attacks someone) to demand that they get access to all the press releases in the same manner that papers that are more supportive or perhaps fairer in their reporting of the news about what the mayor is doing? I don't know of any such right.
Especially not, when they think nothing of "locking" me out from access to commenting on their on-line articles and when I've written to them to ask 'why' -- they ignore my requests.
Especially not, when it feels like they represent a more left-wing, liberal, GBLT agenda than Mayors like Ford may support, or readers like myself.
Especially not, if they can chose what to report and what not to report on local, national, or international.
Especially not, when they chose to fight the mayor on everything he does and everything he does not do. And this baloney about the people have a right to get the news -- garbage. The people get the news from all sorts of sources that present in a much more balanced way.
Why, the Mayor is just using some of their own tactics and they don't like it. Grow up Toronto Star. And take it like a real journal! Sour grapes is not a good colour for your front page.
Or, maybe, just maybe, you need to become a little more humble and apologize to the mayor if he feels you printed lies about him. But no, I guess, you want to stick to your guns. Well, I think he should too.
To our readers -- feel free to share this blog -- pass it on. Enough is enough from these liberal cry babies. Treat the mayor with respect and he'll do likewise.
[Are you looking for a speaker at your church, your club, school, or organization? Ken is available to preach, teach, challenge, and/or motivate. Please contact us.]
Thanks for dropping by. Sign up to receive free updates. We bring you relevant information from all sorts of sources. Subscribe for free to this blog or follow us by clicking on the appropriate link in the right side bar. And please share this blog with your friends. Ken Godevenos, Church and Management Consultant, Accord Consulting.
Sign up (on the right) to receive free updates. We bring you relevant information from all sorts of sources. Subscribe for free to this blog or follow us by clicking on the appropriate link in the right side bar. And please share this blog with your friends and while you're here, why not check out some more of our recent blogs shown in the right hand column.
Also, I've read some good books and make some great recommendations for you at http://astore.amazon.com/accorconsu-20 which you can purchase right from there.
Check our firm out at Accord Consulting.
Finally, if you like what you read here, you may want to donate to my favourite charity, SCA International, by clicking on the logo below. Ken.


text:
Meet the Team
Michael Kron, President
Michael is an accomplished, results-driven senior executive with over 20 years' experience in accounting, negotiations, corporate finance, business development, and strategy. Michael has led and motivated start-up teams through challenges, resulting in many successful outcomes.
Prior to joining AnywhereCommerce, Michael was the Founder/CFO for a number of technology start-ups including mamma.com, a Meta search engine popular in the late nineties, which became NASDAQ listed.
Michael graduated from both McGill University and Concordia University with a bachelor degree in accounting and a CPA degree. He is a member of the Chartered Professional Accountants of Canada and currently sits as an independent director for two public companies on the Toronto Stock Exchange.
Mitchell Cobrin, Founder & Chief Catalyst
Mitchell is a co-founder of AnywhereCommerce and serves to support the overall expansion of the organization. He has nearly 20 years of sales, marketing and high growth experience, with the last decade focused on the electronic and secure payment processing industry. Since the late 90's, his entrepreneurial drive has seen him start up, incubate, grow, sell and consult for a variety of technology companies.
Prior to AnywhereCommerce, Mitchell held the position of VP Sales and Marketing Americas at Keystone Industries until 2000, when he began to pursue his own entrepreneurial objectives by starting MNC Publications (MNCP). MNCP specialized in web marketing and data mining geared for SMBs. In 2005, Mitchell sold MNCP and began laying the groundwork for the company which ultimately became AnywhereCommerce.
Mitchell is a graduate of McGill University, where he majored in industrial relations and business management. Mitchell has twice been nominated for the YE Entrepreneur of the Year Award.
Mark Diamond, VP Strategy
Mark has over 30 years of starting, building, advising, growing and selling companies. Mark is a co-founder of companies that have reached a cumulative public market capitalization of over $800 million. Mark's portfolio includes such leading companies as Gage Applied Sciences, MVS Modular Vision Systems, and Eicon Technologies.
Mark's focus is on business development, product marketing, team building, and financial structuring. He also emphasizes forward thinking in order to see problems and opportunities before they are obvious. His role at AnywhereCommerce is in strategic financial planning as well as taking on special projects ranging from business development to investor relations.
Mark is a graduate of the Harvard Business School, The Wharton School and Choate. Mark lives in Montreal, is married and has one child.
Jeff Park, Senior Director, Partner Sales
Jeff is an accomplished business development and sales executive with nearly 20 years' experience in the payments industry. At AnywhereCommerce, he is responsible for delivery of the companies' leading mobile payment acceptance solutions to acquirers, ISOs and software integrators across North America.
Prior to joining AnywhereCommerce, Jeff was a partner at COMRC, a provider of integrated POS and mobile commerce solutions. He was a sales leader in Verifone's North America Financial Group for more than 12 years, focused on delivering hardware, software, services and integrated solutions to resellers supporting the needs of small and mid-sized merchant businesses.
Jeff holds a BS degree in Accounting and Finance from Miami University.
Jim Poulson, Vice President, Product Strategy & Business Development
Jim is a payment industry veteran, with more than 25 years' experience working for leading hardware, ecommerce, software and enterprise information systems companies.
As VP of Product Strategy, Jim oversees all product development for AnywhereCommerce. This includes managing strategic initiatives related to the company's card readers, mobile software applications, POS systems, and gateway processing platform.
Prior to joining AnywhereCommerce, Jim held senior marketing and business development positions at Verifone, First Data, VivoTech, CyberCash and NCR.
He holds a BS degree in Marketing and Computer Science from Drexel University and a Master of Science in Technology Management degree from Pepperdine University.
Daniel McCann, Chief Technology Officer
Daniel is a seasoned technology executive, investor and entrepreneur, with a 25 year career spanning all aspects of the software ecosystem.
He was the founder and CEO of NetSecure, a mobile payment service provider and pioneer in the field, which sold to AnywhereCommerce in 2017.
He holds a Bachelors of Computer Science from the University of Regina.
Michelle Wagner, Head of Marketing
Michelle manages all aspects of AnywhereCommerce's Marketing activities in her role as an independent contractor. She is a Marketing leader with extensive strategic and hands-on experience in the electronic payments industry. Michelle's knowledge spans all aspects of the business; she has worked for leading companies that deliver terminals and hardware solutions, software and mobile commerce solutions, gateway and e-commerce solutions, and acquiring/processing services.
Prior to working with AnywhereCommerce, she was Senior Vice President, Global Marketing at Elavon where she managed all aspects of Marketing, including the global corporate rebrand that replaced 6 disparate brands.
Michelle was also Director of Global Marketing at Verifone where she defined all aspects of VeriFone's product leadership initiatives and campaigns: positioning, branding, public relations and global launch activities.
Her experience in payments harkens back to the era of early innovators in the payments space, including National Transaction Network (NTN). Michelle managed the product line development and marketing of multi-lane retail electronic payment systems, taking the product from inception to its position as a leading solution for the supermarket industry.
Michelle holds a Bachelor of Business Administration in Marketing from St. Bonaventure University.
Amy Gray, Financial Controller
Amy has five years of experience in the payments industry and nearly 20 years in office and financial administration. At AnywhereCommerce, she manages logistics and the financial health of the company.
Prior to AnywhereCommerce, Amy's experience was in the back offices of many varied industries including restaurants, manufacturing, insurance and travel agencies.
Amy currently lives in Fresno, CA. She has a BA in Art History from the University of New Mexico
Vicki McWeeney, Senior Director of Product Management
Vicki has worked in the electronic payments industry for 25 years and has been focused on mobile payments since 2010. Her industry experience includes product roles at Cardservice International, First Data and Apriva.
In addition to working with mobile payments hardware, she has also managed a mobile payments application. Vicki understands the needs and challenges faced by processors, ISOs and sales agents to launch and support products.
Vicki currently resides in Phoenix, Arizona. She holds a bachelor's degree in Journalism/Public Relations from California State University, Northridge.
Kim Adams, Technical Sales and Customer Support Manager
Kim has been in the Payments Industry for 23 years spending the majority of that time working directly with Product.
As the Technical Sales and Customer Support Manager, Kim is in contact with almost every client making sure that they are set up and trained on the Mobile Payment Application, the Gateway Processing Platform, POS Systems and the Mobile Card Readers. Kim helps to create, update, maintain and distribute documentation to clients and merchants on all aspects of the AnywhereCommerce offerings. She answers and troubleshoots Help Desk emails and phone calls from clients, merchants and vendors as well.
Kim also acts as a Project Manager, working with Sales and newly signed clients that are looking to integrate the AnywhereCommerce Processing Platform into their system.
Prior to joining AnywhereCommerce, Kim worked in various Product Management/Development/Support positions at Vantiv, Ingenico and First Data.
Kim has a Bachelor's Degree in Criminal Justice with a Minor in Human Resources Management from Bellevue University.
Gerardo Mercado, Director of Sales: South America and Caribbean
Gerardo has more than 20 years of experience working with electronic payments solutions. He has led delivery of solutions including Mobile, POS, ATM, ecommerce, gift cards, and others. He has worked with customers in multiple geographical markets including US, Brazil, Mexico, Europe and the Caribbean. Gerardo has played multiple roles including Product Management, Business Development, Marketing and Sales.
Prior to his current role, Gerardo worked for VeriFone as Director of Integrated Systems where he managed delivery of multiple payments systems for customers in Latin America. He served as Business Development Manager and Project Manager at Trintech. Gerardo worked for Hewlett Packard where he managed a Professional Services group that helped deliver payments infrastructure solutions for Banks and Processors.
Gerardo has lived in Austin Texas since the late 1990s. He is fluent in both English and Spanish and currently studies Portuguese. He holds a PMP credential and received his Bachelor degree in Informatics from IPN in Mexico City.
Mauricio Navarro, Director of Sales: Mexico and Central America
Mauricio has more than 17 years of experience in the payment industry in sales and business development. His expertise is focused on the opening of new business markets for the products and services utilized in the payments industry, supporting the growth and positioning of our brand in these regions.
Prior to joining AnywhereCommerce, Mauricio led the Gateway Services division for Mexico at Verifone; worked at First Data in the Business Development department specializing in acquirer and correspondent banking; and at eGlobal with the Operations audit team dealing with its partner banks – Banamex and Bancomer.
Mauricio is a graduate of the University Escuela Bancara y Comercial, where he specialized in Accounting and Business Administration.
Cesar Huerta, Senior Developer & QA: Latin America
Cesar has more than 10 years' experience in the payment industry specializing in development and quality analysis. His efforts as a solution architect and QA manager ensure consistent quality of our products.
Prior to AnywhereCommerce, he worked as QA Manager at the following firms: Verifone, Prosa and Ingenico, where he took the lead on many product roll-outs.
Cesar has a degree in Computer Engineering from the Universidad Nacional Autonoma de Mexico.
Guadalupe Miravete, Sales Representative: Mexico
Guadalupe has more than 30 years of experience in the banking environment.
Before joining AnywhereCommerce, she worked at Verifone in Sales; First Data in Business Development, and 25 years at Banamex, mainly focusing on their Acquirer business.
Guadalupe followed the Technical & Commercial path in her studies at Escuela Bancaria y Comercial.


text:
Photo Gallery
On Saturday, August 26th, 2017 please come out and show your support to the Odessa Fire Company by taking part in our FREE car wash. The car wash will be located at fire station 4 located at 1319 Pole Bridge Road Middletown, Delaware from 10am until 2pm. With easy access to and from Route 1, Route 13, and Route 896 why not come out and bring your dirtiest vehicles for us to get looking good for the weekend. Hope to see you all there!


text:
Corolla S Plus, 4D Sedan, 1.8L I4 DOHC Dual VVT-i, FWD, and Slate Metallic. All the right ingredients! Come to the experts! Be the talk of the town when you roll down the street in this fuel-efficient 2015 Toyota Corolla. This car is nicely equipped with features such as 1.8L I4 DOHC Dual VVT-i, 4D Sedan, Corolla S Plus, FWD, Slate Metallic, 4-Wheel Disc Brakes, 6 Speakers, ABS brakes, Air Conditioning, Alloy wheels, AM/FM radio, Automatic temperature control, Brake assist, Bumpers body-color, CD player, Delay-off headlights, Driver door bin, Driver vanity mirror, Dual front impact airbags, Dual front side impact airbags, Electronic Stability Control, Exterior Parking Camera Rear, Front anti-roll bar, Front Bucket Seats, Front Center Armrest w/Storage, Front fog lights, Front reading lights, Front Sport Bucket Seats, Front wheel independent suspension, Heated door mirrors, Illuminated entry, Knee airbag, Leather steering wheel, Low tire pressure warning, MP3 decoder, Occupant sensing airbag, Outside temperature display, Overhead airbag, Panic alarm, Passenger door bin, Passenger vanity mirror, Power door mirrors, Power steering, Power windows, Radio data system, Radio AM/FM/CD Player w/6.1 Touch Screen, Rear anti-roll bar, Rear seat center armrest, Rear window defroster, Remote keyless entry, Speed control, Speed-sensing steering, Split folding rear seat, Spoiler, Sport Fabric Seat Trim, Steering wheel mounted audio controls, Tachometer, Telescoping steering wheel, Tilt steering wheel, Traction control, Trip computer, and Turn signal indicator mirrors. Ride is compact-car goodness.
Price may exclude tax, title, tags, governmental fees, any emissions testing charges and any finance charges (if applicable). Unless otherwise stated separately in the vehicle details, price does not include documentation, processing, administrative, closing or similar fees. Current mileage may vary due to test drives and vehicle relocation.