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Heart Disease
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The heart is a miracle of intricacy and elegance. This fist-sized organ, weighing less than a pound, beats 72 times a minute–more than 100,000 times a day–pumping from 2,500 to 5,000 quarts of blood through some 75,000 miles of blood vessels (almost 3 times around the earth at the equator), to nourish the 100 trillion or so cells that the body contains. This goes on 24 hours a day, 7 days a week, with no breaks or vacations for 70 to 100 years, or until something happens to throw off the rhythm, (to delay or halt the heartbeat, to prevent blood from reaching its destination).
The most commonly heard heart term, cardiac, comes from the Greek kardia. The possible first use of this Greek word for cardiac or heart goes back about 2,300 years to the era of the Greek philosopher Aristotle (384-322 B.C.). The father of Aristotle was a noted physician by the name of Nicomachus. This familial tie prompted Aristotle to study anatomy and disease under Plato. After observing the activity of an embryonic heart in an incubating egg, it was Aristotle who named the largest artery in the body: aorta. Subsequently, Aristotle tutored Alexander the Great, who later conquered Egypt and founded the city of Alexandria, which became a world center of science and medicine. The physician Erasistratos founded a school of anatomy and, by dissection, he discovered the heart consisted of four separate chambers.
The harsh fact is, cardiovascular diseases (CVD) are the leading killer of women and men. These diseases cause about a death a minute among females–claiming nearly half a million female lives every year. That’s more lives than the next 7 causes of death combined. Starting at age 75, the prevalence of CVD among women is higher than among men. Coronary heart disease rates in women after menopause are 2-3 times those of women the same age before menopause. Heart disease is more deadly than all other modern scourges combined, including cancer and loss of life from car accidents, crime and war. Cancer is next, at about 20% of all deaths and deaths from diabetes adds another 5%. In the United States, cardiovascular disease is responsible for almost as many deaths as all other causes of death combined. Almost one of every two deaths in the U.S. are due to CVD.
Since 1900 CVD has been the No. 1 killer in the United States every year but 1918. Nearly 2,600 Americans die of CVD each day, an average of 1 death every 34 seconds. CVD claims more lives each year than the next 5 leading causes of death combined, which are cancer, chronic lower respiratory diseases, accidents, diabetes mellitus, and influenza and pneumonia. Of the 64,400,000 Americans with one or more types of cardiovascular disease, 25,300,000 are estimated to be age 65 and older. 50,000,000 have high blood pressure; 13,200,000 have Coronary heart disease; 7,800,000 have myocardial infarction (heart attack); 6,800,000 have angina pectoris (chest pain); 5,000,000 have congestive heart failure; 4,800,000 have stroke; 1,000,000 have congenital cardiovascular defects; 1 in 5 males and females has some form of CVD. In 2001 an estimated 6,188,000 inpatient cardiovascular operations and procedures were performed in the United States; 3.6 million were performed on males and 2.6 million were performed on females.
CVD accounted for 38.5 percent of all deaths or 1 of every 2.6 deaths in the United States in 2001. CVD mortality was about 60 percent of “total mortality.” This means that of over 2,400,000 deaths from all causes, CVD was listed as a primary or contributing cause on about 1,408,000 death certificates. The CDC estimates that each year 400,000 to 460,000 people die of heart disease in an emergency department or before reaching a hospital, which accounts for over 60 percent of all cardiac deaths. This year an estimated 700,000 Americans will have a new coronary attack. About 500,000 will have a recurrent attack. The average age of a person having a first heart attack is 65.8 for men and 70.4 for women. Almost 150,000 Americans killed by CVD each year are under age 65. The lifetime risk of developing CHD after age 40 is 49 percent for men and 32 percent for women. The incidence of CHD in women lags behind men by 10 years for total CHD and by 20 years for more serious clinical events such as myocardial infarction (MI) and sudden death.
CVD ranks as the No. 3 cause of death (behind certain conditions originating in the perinatal period and accidents) for children under age 15. And in 2001 about 197,000 cardiovascular procedures were performed on people age 15 or younger. In the next twelve months 25,000 babies will be born with congenital heart defects. About one-fourth of these infants will die, and the survivors will join the nearly half-million persons with heart defects still living. These defects claim more lives than any other kind of congenital defects–about 2,200 lives a year of children under age 15. Most CVD in children is due to congenital cardiovascular malformations, but children can develop other forms of CVD, such as high blood pressure and end-stage renal disease. And that’s not all.
• In 2000 in the United States, about 1,300 hospitalizations were for children under age 20 with acute or subacute bacterial endocarditis; 600 with acute myocarditis; 1,500 with acute pericarditis; and 2,600 with chronic pericarditis.
• About 7,700 hospitalizations were for children with arrhythmia, including 5,000 with supraventricular tachycardia and 2,700 with ventricular tachycardia.
• About 4,800 hospitalizations were for children with cardiomyopathy, and 400 with hypertrophic cardiomyopathy.
• About 150 hospitalizations were for children with acute rheumatic fever including carditis, and 1,900 chronic rheumatic fever.
• Kawasaki disease, an inflammatory disease that occurs nearly exclusively in children, can result in coronary artery damage if not treated promptly. In 2000 there were about 4,300 hospitalizations for Kawasaki disease.
Stroke among children is a serious and largely unrecognized problem, killing many and leaving others with often severe deficits. Strokes in children occur disproportionately in infants, particularly among those under age 1. Cardiovascular diseases exact a devastating toll on our kids. The statistics above only hint at the problem. At New York University Medical Center, Mildred S. Seelig, M.D. has been investigating atherosclerosis and other heart conditions in thousands of children and infants under two-and-a-half years of age. In a recent report to her medical colleagues, she concluded: “The cardiovascular diseases of infancy and childhood that are common enough to require specialty medical care and surgical correction are a development of the past 30 to 40 years, as is the epidemic of sudden death of men under fifty from ischemic heart disease (IHD). Less widely recognized is the evidence that sudden death from IHD has also occurred in infancy and childhood, with increasing frequency during the same period of time, as has generalized arteriosclerosis in very young infants, and atherosclerosis, hyperlipemia, and hypertension in older infants and children. The initial cardiovascular lesion can begin early in life.”
Certain types of blood flows may cause mechanical damage to the blood vessels. These types of blood flows are referred as injurious pulsatile flow. In response to this mechanical injury, the vessel develops plaques and abnormalities in the vessel wall in a predictable pattern. The presentation of these various mechanisms in a unified concept is called the protective adaptation theory. This theory provides the missing link, particularly in events preceding lesion development, where current biochemical theories cannot account for the mechanisms. Endothelial injury is caused by a high-intensity stimulus over a short period of time, i.e., a coronary artery stent placement. Stress is caused by a low-intensity stimulus over a long period to time, i.e., a callus is a standard adaptation of the skin to stress. A key difference between protective adaptation to stress and to injury is that protective adaptation to stress is usually reversible.
Blood behaves very differently in our circulatory system than water flowing in pipes. First of all, blood has a higher viscosity (thickness) than water. Increased blood viscosity and blood flow is pulsatile and the flow rate varies with time. The reason for the pulsatile flow is two-fold, a resultant of the ejection portion of the cardiac cycle and because the arterial wall is elastic. The arterial system is not a straight pipe with its many bifurcations and bends. Pulsatile blood flow imparts energy into the arterial system that is stored partially in the blood vessels. The protective adaptation process theory organizes the arterial system’s adaptative process into two cycles, both of which originate from the mechanical stresses in the system. The first cycle is the region-specific development of arteriosclerosis, a condition in which the arteries have lost their compliance (elasticity). The second cycle is site-specific development of atherosclerosis in arteries that lost their compliance in cycle one. Although, arteriosclerosis is a precursor to atherosclerosis, the two cycles develop synergistically and reinforce each other in a vicious circle.
At birth, arteries are extremely compliant and stretchable, but over a lifetime these characteristics decrease as a result of the changes in wall tissue structure. The loss of compliance has been defined as medial arteriosclerosis. The changes of compliance in the arterial wall is an adaptative response to the stretching and stress of high arterial pressure, which causes extended, repeated over-stretching of the arteries. Atherosclerosis is an adaptive response that leads to arterial occlusive disease. Starting as a response to the mechanical injury of endothelial cells, atherosclerosis occurs at very specific sites in the arterial system. The frequency of atherosclerosis in these specific sites correlates with their exposure to injurious systolic pressures and repeated stretch-recoil processes. This explains why the arteries leading from the heart and brain are so susceptible to atherosclerosis.
Viscosity represents the stickiness and thickness of blood. It is the frictional resistance to blood flow. So as blood viscosity increases, blood flow decreases assuming that the heart maintains the same systolic pressure. In order for the heart to maintain the same cardiac output, the systolic pressure must increase as the whole blood viscosity increases. Elevated blood viscosity contributes to the arteriosclerosis, atherosclerosis and increased peripheral vasculature resistance. Increased vasculature peripheral resistance results in hypertention and an increased left ventricle requirement ot work harder. Eventually the atherosclerosis narrows the lumens (inside diameter) in the vessels and the blood pressure gradients increase inversely proportional to the 4th power of the lumen’s decreased diameter size. Only 25 - 35% of the left ventricular ejection flows directly to the peripheral vessels from the arterial system to the veins. As blood viscosity and peripheral vasculature resistance increases, an even large volume remains a “pulsatile mass” hammering the arterioles (greatest pressure gradient) very similar to the “water hammer” effect in water supply pipes.
Fibrinogen is a major determinant of both plasma and whole blood viscosity. One of the logical and practical ways to reduce whole blood viscosity is to remove fibrinogen from the blood. Lowering fibrinogen levels limits red cell aggregation and reduces whole blood viscosity and plasma viscosity, especially at lower shear rates.
Within several months of birth, abnormal physiological changes begin to take place within the circulatory systems of most infants. Tiny injuries to the endothelial linings of the medium and larger arteries develop, possibly as the result of turbulent blood flow caused by deficient metabolized foodstuffs. As a result of these injuries, blood platelets begin to accumulate, along with isolated monocytes and macrophage foam cells, and begin to fill in with excess cholesterol and fats. By about age three and through age ten in many children eating the modern diet, the lipid-filled monocytes and macrophage foam cells have formed into clusters, and fatty streaks begin to appear on smooth muscle cells on the inside lining of the aorta and other arteries. At first, the streaks localize around the openings of arteries, especially where they branch into connecting blood vessels. In the next decade of life, the fatty streaks progressively increase, and many teenagers develop raised lesions in their arteries exhibiting necrosis and other degenerative changes. Cholesterol, fat and other sticky substances are also attracted to minor injuries in arterial walls that arise from high blood pressure. The aorta and coronary arteries, where the pressure is highest, are especially susceptible to injury and accumulation of intra- and extracellular lipids. By the early twenties–though in some cases sooner and in others later–raised lesions in the aorta and coronary arteries turn into fibrous plaque. As cholesterol and fat build up, they become encapsulated by scar-like fibrous tissue that binds them firmly to arterial walls.
Plasma proteins such as fibrin and fibrinogen also accumulate in atheromata. Meanwhile, tiny blood vessels in the artery walls continue to supply more fat and cholesterol to fibrous tissues so that the deposits continue to grow. Like sediment in a riverbed, layers of fat, cholesterol, protein and minerals coagulate and change from soft, spongy clusters to hardened, rocklike strata. It is estimated that atheromata spread or develop over the surface area of the major blood vessels, especially the coronary arteries, at the rate of about 2% a year in persons on our diets. By the mid-thirties and early forties, the atherosclerotic deposits in many people have calcified, as chalky minerals fill in the fibrous scar tissue. Most young adults have plaque not only in the heart vessels but also along the entire length of the ascending aorta, leading toward the brain, and along the iliac and femoral arteries nourishing the organs in the pelvic region. These complicated lesions set the stage for stroke, heart attack or peripheral vascular disease. Usually, the plaque obstructs only a part of the arterial opening, which is called the lumen.
Oxygen supply is generally not threatened until 50% of the lumen is blocked, though in some cases, heart attack can occur with only minimal narrowing of the coronary vessels. To compensate for the diminished supply of oxygen, the heartbeat, cardiac output, and blood pressure tend to rise. When about 70% of the coronary arteries are occluded, or obstructed, severe pain and discomfort may arise in the chest area and be felt radiating to the neck and down one or both arms. This chronic chest pain, which reaches a threshold at certain levels of activity, is called angina pectoris. Partial or total narrowing of the coronary arteries by the buildup of plaque or the formation of blood clots can cause a myocardial infarction in the heart or a cerebral infarction in the brain. By the onset of a heart attack or angina, two or three main vessels in the coronary circuit are usually obstructed by deposits. In addition to narrowing the arteries, atherosclerotic plaque may ulcerate and form thrombi made up chiefly of coagulated blood platelets.
These blood clots may form when blood circulation is slowed, or they may develop around atheromata and further obstruct the arteries. Blood clots may also be swept away by a surge of elevated blood pressure or other motion and lodge in distant parts of the circulatory system. From the lining of the aorta, neck vessels, and coronary arteries, thrombi can develop and be propelled up to the brain or down to the legs and feet. An embolus, or detached thrombus, will continue to drift to smaller-diameter blood vessels where it may eventually become lodged like a boulder in a stream. When this happens, blood supply may be completely shut off, producing an infarction, or localized death, of a segment of the brain, the heart muscle, the legs or the feet. Other complications may also result from the buildup of atherosclerotic plaque. When tissue in the wall of an artery under an atheroma bleeds, hemorrhaging may result. An abscess, or localized infection, may also develop beneath the hardened deposit, leading to injury and disease.
During the Vietnam War, doctors examined the bodies of American soldiers killed in combat to determine the cardiovascular condition of relatively healthy and active young males. Autopsies showed that 45% had some evidence of coronary atherosclerosis and 26% showed hardening in more than one heart vessel. The average age of the young men was 22. In 2004 the estimated direct and indirect cost of CVD is $368.4 billion. In 1999, $26.3 billion in program payments were made to Medicare beneficiaries discharged from short-stay hospitals, with a principal diagnosis of cardiovascular disease. That was an average of $7,883 per discharge. Heart attacks are only one form of cardiovascular disease, which include hypertension (high blood pressure), coronary heart disease, rheumatic heart disease, and stroke (among others).
Angina Pectoris
Angina pectoris is chest pain or discomfort due to insufficient blood flow to the heart muscle. Stable angina is predictable chest pain on exertion or under mental or emotional stress. Significantly more women than men have angina, both in total numbers and as an age-adjusted percentage. A study of four national cross-sectional health examination studies found that, among Americans ages 40-74, the age-adjusted prevalence of angina pectoris (AP) was higher among women than men. Only 20 percent of coronary attacks are preceded by longstanding angina. The percentage is lower if the infarction is silent or unrecognized. A small number of deaths due to coronary heart disease are coded as being from angina pectoris. These are included as a portion of total deaths from CHD.
Coronary Heart Disease
Coronary heart disease (CHD) is the single largest killer of American males and females. About every 26 seconds an American will suffer a coronary event, and about every minute someone will die from one. About 42 percent of the people who experience a coronary attack in a given year will die from it. About 340,000 people a year die of CHD in an emergency department (ED) or before reaching a hospital. Most of these are sudden deaths caused by cardiac arrest, usually resulting from ventricular fibrillation.
In 2001 the overall CHD death rate was 177.8 per 100,000 population. 84 percent of people who die of CHD are age 65 or older. About 80 percent of CHD mortality in people under age 65 occurs during the first attack. 25 percent of men and 38 percent of women will die within 1 year after having an initial recognized MI. In part because women have heart attacks at older ages than men do, they’re more likely to die from them within a few weeks. Almost half of men and women under age 65 who have a heart attack (MI) die within 8 years. The estimated average number of years of life lost due to a heart attack is 11.5. Fifty percent of men and 64 percent of women who died suddenly of CHD had no previous symptoms of this disease. Between 70 and 89 percent of sudden cardiac deaths occur in men, and the annual incidence is 3 to 4 times higher in men than in women. However, this disparity decreases with advancing age. People who’ve had a heart attack have a sudden death rate that’s 4-6 times that of the general population. Sudden cardiac death accounts for 19 percent of sudden deaths in children between 1 and 13 years of age and 30 percent between 14 and 21 years. The overall incidence is low, 600 cases per year.
Depending on their gender and clinical outcome, people who survive the acute stage of a heart attack have a chance of illness and death that’s 1.5-15 times higher than that of the general population. The risk of another heart attack, sudden death, angina pectoris, heart failure and stroke–for both men and women–is substantial. Within 6 years after a recognized heart attack 18 percent of men and 35 percent of women will have another heart attack, 7 percent of men and 6 percent of women will experience sudden death, about 22 percent of men and 46 percent of women will be disabled with heart failure, 8 percent of men and 11 percent of women will have a stroke. About two-thirds of heart attack patients don’t make a complete recovery, but 88 percent of those under age 65 are able to return to their usual work. The outlook for people who have an unrecognized attack is about the same or worse. CHD is the leading cause of premature, permanent disability in the U.S. labor force, accounting for 19 percent of disability allowances by the Social Security Administration.
Acute Coronary Syndrome
The term acute coronary syndrome (ACS) is increasingly used to describe patients who present with either acute myocardial infarction or unstable angina (UA). (Unstable angina is chest pain or discomfort that’s unexpected and usually occurs while at rest. The discomfort may be more severe and prolonged than typical angina or be the first time a person has angina.) 928,000 is a conservative estimate for the number of people with ACS discharged from hospitals in 2001. When including secondary discharge diagnoses, the corresponding number of hospital discharges was 1,680,000 unique hospitalizations for ACS, 959,000 for MI and 758,000 for UA (37,000 hospitalizations received both diagnoses).
If you’re a male and 20 years old, and have been on the Basic American Diet all your life, the odds are that all three of your coronary arteries average 20% closure. You’re in the early stages of heart disease. If you’re over 20 years old, you’re undoubtedly not healthy at all; statistically, you are well on your way to suffering severe heart disease. If you’re female and 30, the odds are that you’re as sick as a 20-year-old man with all three arteries 20% closed. You’re lagging 10 years behind men on the road to heart disease, but you’ll catch up after menopause. If you’re a male and 35, the odds are that all three coronary arteries average 50% closure, although you still feel well. Even if all three of your coronaries were 65% closed, you could pass the most vigorous stress treadmill test and be told that you are healthy. Until at least one of your coronary arteries is 90-100% closed, you have no symptoms. But now you might have some chest pressure upon activity. Now you might have a heart attack. Now you could suddenly die while running.
Since ancient times, enzymes have unknowingly been involved in treating human ailments. While the properties of enzymes have largely been unknown until recently, results were witnessed and associations of health or disease were made between various plant and animal substances. The healing properties of herbs are primarily attributed to alkaloid or other chemical properties that trigger a response in the body. Invariably, the chemistry of herbs affects metabolic enzyme pathways. The unique substance either inhibits an enzyme or stimulates another to change body chemistry. Some plants have unique essential oils capable of inhibiting or destroying pathogenic microorganisms due to the disruption of some enzymatic pathway of the organism. Regardless of what healing modality is chosen, what remains to be understood is that in every case the healing can only occur if the body has enough metabolic enzymes to do the work. Work in this case denotes the ability to initiate, alter, speed up or slow down biochemical processes. It indicates having the capacity to break apart or join together components synergistically, to change their original structure and function.
Doctors pay lip service to a "healthy diet" and exercise as cardio-preventive measures. Dieticians have even worked out a "food pyramid" to help us make wise eating choices. Yet, in spite of the best intentions, the death rate continues to rise and there is no chance of its diminishing in the near future based on the models we have. The food industry "fortifies" food with some 11 "esential" nutrients (synthetic coal-tar derivatives) including B vitamins, calcium, magnesium, potassium, iron and sodium. Yet, the very substances that would digest the food are deliberately left out, destroyed for the sale fo extended shelf life.
At the beginning of the 20th century, the transportation of food across a continent posed serious problems. How could a company ship raw, uncooked food without spoilage? The answer was to find a way to process the food and ship it without rotting. In the early 1900s, salicylic acid (aspirin) was used because it prevented the action of enzymes. So, as early as 1903, aspirin was known to affect enzymes. It was used in this way to preserve food for extended shelf-life. As newer techniques for extending the shelf-life were discovered, aspirin was discontinued. Is it not absurd, then, knowing how aspirin destroys most enzymes, that many patients are told to take aspirin in the prevention of heart disease? Salicylic acid has a disintegrating action on the blood cells. The blood-thinning properties of aspirin result from the fact that it destroys red blood cells, causing fewer of them to be found in the bloodstream!
The medical explanation of cardiovascular disease fails to explain the picture fully because it is missing the major piece of the puzzle. Medical research is funded with billions of dollars to find the "cure." In spite of this, triple-bypass surgery is covered by insurance while the advice and wisdom of nutritionists is not. Prevention is not practiced because it does not bring in the revenue that surgery, radiation and drugs do.
Much attention is paid to markers of potential heart disease. The category of lipoproteins is a good example. Lipo means "fat," and protein is self-explanatory. The four principal classes are: high density (HDL), low density (LDL), very low density (VLDL) and chylomicrons. Chylomicrons are dietary triglycerides. VLDLs are endogenous (from within the body) triglycerides, while LDL and HDL are both endogenous cholesteryl esters. Lipoproteins are necessary for the transport of lipids (fats). We are told it is healthy to have relatively high HDL levels, but should have low cholesterol (LDL), VLDL and triglyceride levels.
The endogenous group of lipoproteins is manufactured within the body, but the raw material is still derived from the fats and proteins we consume. Food must be digested in order for the body to utilize it. The abnormal accumulation of lipoproteins in the blood in a small percentage of the population represents an autosomal dominant genetic trait. But, in the majority of people with cardiovascular issues, it is evidence of incomplete digestion of fats and protein--accompanied by the fact that people simply overeat. How can the body properly eliminate unused fats and protein when there simply is too much being taken in? The body must hide or store this unusable waste. Some of it is stored in tissue and some of it circulates. When the kidnesy and colon cannot eliminate enough waste, the skin compensates. The skin is the largest eliminative organ. Skin eruptions are the attempt to rid the body of waste.
Unfortunately, what circulates begins to adhere to the walls of the blood vessels, clogging them up. Macrophages are summoned to remove this accumulation, but cannot do so without an adequate supply of enzymes. Enzymes produced by the macrophages for their immune function are used for digesting the cooked food. Obviously, this prevents the breakdown of lipoproteins which continue to build up. Foam cells associated with atherosclerosis are formed when overaccumulation of fats occurs in macrophages.
The accumulation transpires because cooked foods are not completely digested in the stomach. These undigested remnants cross the intestinal border into the blood and lymph, circulating throughout. Over time, their accumulation leads to damaged arterial tissue. Macrophages cannot break down the lipoprotens due to the exhaustion of their own enzymes. Eating cooked fats demands enzymes in digesting them. Cooked foods must be broken down, even at the expense of the cardiovascular system. This daily assault of cooked foods drains lipase from many sources, especially the immune and lymph systems.
Plant enzymes taken before meals completely digest food. Therefore, no remants can cross over into the blood. Having prevented further accumulation of undigested food, one can focus on removing the accumulated material. Enzymes taken between meals are taken up by the body and sent to work in areas that need them the most. Enzymes will digest the undesirable lipoproteins in the blood vessels without affecting the vessels themselves. Reversal of cardiovascular disease is a matter of improving digestion and modifying dietary stress factors--in this case, fats and proteins.
Fibrin is a protein that forms in the blood after trauma or injury. This is essential to stop excess blood loss. There are more than twenty enzymes in the body that assist in clotting the blood, while only one that can break the clot down (plasmin). Bacteria, viruses, fungi and toxins present in the blood also trigger an inflammatory condition resulting in excess cross-linked fibrin. Since there is no danger of blood loss and trauma has not occurred, this cross-linked fibrin will circulate through the blood and will stick to the walls of blood vessels. This contributes to the formation of blood clots, slows blood flow and increases blood viscosity contributing to the elevation of blood pressure. In the heart, blood clots cause blockage of blood flow to heart muscle tissue. If blood flow is blocked, the oxygen supply to that tissue is partially cut off (ischemia) which results in angina and heart attacks, or if prolonged, death of heart muscle (necrosis). Clots in chambers of the heart can mobilize to the brain, blocking blood and oxygen from reaching necessary areas, which can result in senility and/or stroke.
Thrombolytic enzymes (enzymes that break down blood clots) are normally generated in the endothelial cells of the blood vessels. As the body ages, production of these enzymes begins to decline, making blood more prone to coagulation. This mechanism can lead to cardiac or cerebral infarction, as well as other conditions. Since endothelial cells exist throughout the body, such as in the arteries, veins and lymphatic system, poor production of thrombolytic enzymes can lead to the development of blood clots and the conditions caused by them, virtually anywhere in the body. It has recently been revealed that thrombotic clogging (blood clots) of the cerebral blood vessels may be a cause of dementia.
Thrombotic diseases typically include cerebral hemorrhage, cerebral infarction, cardiac infarction and angina pectoris, and also include diseases caused by blood vessels with lowered flexibility, including senile dementia and diabetes. If chronic diseases of the capillaries are also considered, then the number of thrombus related conditions might be much higher. Cardiac infarction patients may have an inherent imbalance. Their thrombolytic enzymes are weaker than their coagulant enzymes.
Recently a new enzyme with potent fibrinolytic activity, that rivals pharmaceutical agents, has been discovered and shows great potential in providing support for hypercoagulative states and in supporting the activation of many of the body’s 3,000 endogenous enzymes. Dr. Sumi, a professor in the Department of Chemical Technology, College of Science and Industrial Technology, Kurashiki University of Science and the Arts, has clarified the beneficial effects of isolated, purified and encapsulated nattokinase, an enzyme derived from boiled soybeans and Bacillus natto, called natto, pronounced “nah-toe.” Natto, which has recently attracted attention throughout the world, is a familiar part of the Japanese diet. Japan has the highest average longevity in the world, which is partly attributed to a high consumption of cultured soybean products, especially “natto.”
In the US, Dr. Sumi found that the sticky part of natto, commonly called “threads”, exhibited a strong fibrinolytic activity. He named the corresponding fibrinolytic enzyme nattokinase in 1980. Dr. Sumi conducted research on about 200 kinds of food from all over the world, and he found that natto had the highest fibrinolytic activity among all those foods.
The most distinctive features of natto are the adhesive surrounding the soybeans and the strong flavor. The sticky material has been shown to consist of poly-g-glutamic acid (D and L) and polysaccharides (levan-form fructan) and the strong “cheese-like” flavor is due to the presence of pyrazine. These are the main factors which give natto the outstanding properties.
Nattokinase may actually be superior to conventional clot-dissolving drugs costing many times more, such as recombinant tissue plasminogen activators (rt-PA), urokinase, and streptokinase, which are only effective therapeutically when taken intravenously within 12 hours of a stroke or heart attack. Nattokinase, however, may help prevent the conditions leading to blood clots with an oral daily dose of as little as 2,000 fibrin units (FU) or 50 grams of natto. Moreover, the efficiency of a fibrinolytic injection lasts only 4 - 20 minutes, whereas nattokinase maintains its activity for 4 - 12 hours.
Natto-kinase supports patients with thrombotic conditions in a convenient and consistent manner, in several different ways, without side effects. Nattokinase produces a prolonged action in two ways: it prevents the formation of thrombi and it dissolves existing thrombus. Oral administration indicates elevations of the breakdown products of the fibrin and the ability of the blood to breakdown fibrin called euglobulin fibrinolytic activity (EFA). Fibrinogen degradation products (FDP) levels in adults drastically increase 4 hours after the administration of the nattokinase indicating that fibrin within the blood vessels is gradually being dissolved with repeated intake of nattokinase. By measuring EFA & FDP levels, the activity of nattokinase has been determined to last form 8 to 12 hours. After oral administration of nattokinase there is a rise in blood levels of tissue plasminogen activator (TPA) antigen, which indicates a release of TPA from the endothelial cells and/or the liver and the endogenous production of plasmin (the body’s blood clotting buster).
In studies in Japan on both animal and human subjects, researchers confirmed the presence of inhibitors of angiotensin converting enzyme (ACE) within the test extract of lyophilized viscous materials of natto. ACE causes blood vessels to narrow and blood pressure to rise—by inhibiting ACE; nattokinase has a lowering effect on blood pressure. Blood pressure levels were measured after 30 grams of lyophilized extract (equivalent to 200 grams of natto food) was administered orally for 4 consecutive days. In 4 out of 5 volunteers, the systolic blood pressure (SBP) decreased an average drop of 10.9% and diastolic blood pressure (DBP) decreased an average drop of 9.7%.
Nattokinase has many benefits including convenience of oral administration, confirmed efficacy, prolonged effects, cost effectiveness, and can be used preventatively. It is a naturally occurring, food dietary supplement that has demonstrated stability in the gastrointestinal tract. Only nattokinase acts only on the fibrinolytic system to dissolve thrombi within the blood vessels.
Research has shown nattokinase to support the body in breaking up and dissolving the unhealthy coagulation of blood and to support fibrinolytic activity. Already, backed by strong and novel research, Nattokinase shows promise in supporting areas such as cardiovascular disease, stroke, angina, venous stasis, thrombosis, emboli, atherosclerosis, fibromyalgia/chronic fatigue, claudication, retinal pathology, hemorrhoid, varicose veins, soft tissue rheumatisms, muscle spasm, poor healing, chronic inflammation and pain, peripheral vascular disease, hypertension, tissue oxygen deprivation, infertility, and other gynecology conditions (endometriosis, uterine fibroids).
Recently, the incidence of osteoporosis is increasing dramatically. One cause of osteoporosis is a lack of Vitamin K2. Natto contains plenty of Vitamin K2, and may therefore help to control the aging process. In the US, an isophrabon compound, one of the antioxidants in natto, is considered promising for the prevention of prostate cancer and breast cancer. Another component of natto, di-picolinic acid, has an antibacterial effect, and helps to prevent the viral infection of O-157, which controls the intestinal environment by increasing useful bacteria.
In a coronary bypass surgery, surgeons take a segment of a healthy blood vessel from another part of the body and make a detour around the blocked part of the coronary artery.
* An artery may be detached from the chest wall and the open end attached to the coronary artery below the blocked area.
* A piece of a long vein in your leg may be taken. One end is sewn onto the large artery leaving your heart -- the aorta. The other end of the vein is attached or "grafted" to the coronary artery below the blocked area.
* Either way, blood can use this new path to flow freely to the heart muscle.
A patient may undergo one, two, three or more bypasses, depending on how many coronary arteries are blocked. Cardiopulmonary bypass with a pump oxygenator (heart-lung machine) is used for nearly all coronary bypass graft operations. This means that besides the surgeon, cardiac anesthesiologist and surgical nurse, a competent perfusionist (blood flow specialist) is required. Studies published in the 1990s in the Journal of the American Medical Association, the New England Journal of Medicine and reports by the U.S. government show that between 50% and 90% of bypass surgeries (and also angioplasties) are not only unnecessary, but do not result in increased survival. This operation, performed some 500,000 times each year in the United States, does not cure patients, it is scandalously overused, and its high cost drains resources from other areas of need.
Fully half or more of the bypass operations performed in the United States are unnecessary. A decade of scientific study has shown that except in certain well-defined situations, bypass surgery does not save lives, or even prevent heart attacks. Yet many American physicians continue to prescribe surgery immediately upon the appearance of angina, (chest pain). In the United States in 2001, the NCHS estimates that 516,000 of these procedures were performed on 305,000 patients.
Physicians immediately embraced the idea of coronary-bypass surgery when the procedure was introduced in 1967–even though no evidence of its benefits was yet available. By 1969 the procedure was being performed at most of the nation's major medical centers. By the mid-1970s the number of surgeons trained to do bypass surgery was increasing at a rate of 10% to 15% each year, and as these new surgeons sought out suitable locales to practice their trade, the number of hospitals doing cardiac surgery just about doubled. Almost every small city in America now has a surgical team competing with the older referral centers, and any hospital aspiring to be a "complete medical center" seeks to have a team of its own--not just for prestige but because the operation is the biggest revenue-producer in the health field.
Coronary-bypass surgery consumes more of our medical dollar than any other treatment or procedure. The average cardiac surgeon's fee in the United States is between $4,500 and $5,000 per bypass operation. The range is from $2,000 (for welfare patients done under contract) to more than $15,000. In high-rent districts fees routinely run from $7,000 to $10,000. Some surgeons operate three times a day, perhaps 700 times a year, using assistants to do the opening and closing. Their incomes are in the millions. But the head surgeon isn't the only one with a direct economic stake in the bypass operation. In most hospitals one or two "assistant surgeons" each get an additional 20% of the head surgeon's fee--even though most of the tasks that they perform could be done by interns, nurses, or non-medical assistants. And a surgeon receives fees for being on call, while a cardiologist performs a potentially hazardous procedure. If the surgeon isn't needed, he gets $500 to $800 for "availability."
Cardiologists also profit handsomely from the bypass operation, by doing the associated diagnostic work. The basic test is a cardiac catheterization, in which dye is injected into the coronary arteries to determine how severe and how many are the obstructions. The professional fee averages $800, not quite in the surgeon's ballpark; but a cardiologist may do two or three catheterizations for every patient sent to surgery--and performing even five a week can generate an annual income of $184,000, while consuming only a fifth of his time. Anesthesiologists, who also derive fees from bypass surgery, tend to have complicated schedules based on time spent, and their fees vary from place to place. But the national average is about $1,250 per case, and since responsibilities before and after the operation are minimal, the average anesthesiologist can handle two cases everyday with ease. Then there's the hospital. For the diagnostic cardiac catheterization alone, lab and technicians' fees average $1,100. Charges for other tests and for hospital stay are additional (intensive-care units average $1,000 a day, plus extras). Operating-room fees (for nurses, technicians, equipment, and supplies) run from $5,000 to $8,000. The usual blood tests, X-rays, and scans bring the total costs for one bypass operation to about $25,000. Of this, various physicians fees are about $7,500, or nearly 30% of the total. These are averages; in some cases, the total charges exceed $100,000.
Patients who are given the bypass operation "to prolong life" fall into four major groups, only one of which has ever been shown to gain the promised result of such surgery. The first group is composed of those who suffer no symptoms at all. A second likely candidate for bypass surgery is the patient who has just suffered or recovered from a heart attack. Some cardiologists recommend the operation for all such patients, hoping that it will protect against another heart attack or sudden death. A third contender for the scalpel is the patient who appears to be having a heart attack. The signs of an impending heart attack are notoriously unreliable --about two out of three patients admitted to hospitals for possible heart attacks turn out not to have had them. Bypass surgery cannot possibly prevent heart attacks in those who aren't having them. About 11 % of all bypass operations are performed on heart patients for whom surgery clearly prolongs life--those suffering an obstruction of the left main artery. Another 10% of patients, who have obstructions of all three major coronary arteries plus a weakened heart muscle, might have some extension of life owing to surgery, but we won't know if this is so until many more years have passed.
Heart Bypass Surgery Linked to Mental Decline
Five years after heart bypass surgery, 42% of patients show a significant decline on tests of mental ability, probably from brain damage caused by the surgery, doctors from Duke University say, in a study published in the New England Journal of Medicine. The study highlights an ugly truth that surgeons know, but are usually reluctant to discuss with patients. Some patients are mentally impaired after bypass surgery. Doctors suspect various factors that interfere with cerebral blood flow during surgery are to blame.
The findings are just the latest research to question whether most of the nearly 500,000 bypass operations performed each year in the United states are necessary. Studies published in the 1990s in the Journal of the American Medical Association, the New England Journal of Medicine and reports by the U.S. government show that between 50% and 90% of bypass surgeries (and also angioplasties) are not only unnecessary but do not result in increased survival. This study is not the first to link mental decline to bypass operations. But earlier studies were shorter term, and many doctors hoped that the cognitive losses would be temporary.
The new study is the first to show lasting changes in so many patients so long after the surgery. The patients’ average age was 61, with a range of 50 to 71. The drop in scores in the bypass patients could not be attributed to aging, the authors said, because it was more than two to three times the mental decline found in patients who did not have bypass surgery and whose cognitive abilities were followed for five years in a separate study. Several elements of bypass surgery can potentially cause brain damage.
One is the heart-lung machine, through which the patient’s blood is circulated to pick up oxygen. Bubbles produced by the machine may block blood flow through minute vessels in the skull, killing brain cells. The machine may also send droplets of fat released from the surgical site to the brain, where they can cause the same damage as the air bubbles. It is also possible that the machine does not provide enough oxygen for some patients. The other possible source of trouble is fatty deposits inside the patient’s aorta, the large vessel that carries blood out of the left side of the heart. Surgeons clamp the aorta and may sew blood vessels to it during bypass surgery; these procedures can break off fatty deposits, which may then travel to the patient’s head and block blood flow.
Heart-lung Bypass Pump
When it comes to heart surgery, some surgeons are bypassing heart-stopping bypasses in favor of “off-pump” procedures. For decades, bypassing blocked arteries has required the patient’s heart to be still. While the surgeon works, grafting a new vessel around the blocked artery, a heart-lung machine—or pump, as it’s often called—circulates oxygen-enriched blood through the rest of the body. The heart, stopped with a chemical solution, lies inert and bloodless as the surgeon sews, connecting vessels often not much wider than a single strand of spaghetti.
A technique developed a decade ago, called off-pump, or beating heart surgery, allows the heart to pump throughout the operation. With the use of stabilizing devices, the area of the heart to be bypassed—usually about one inch square—is immobilized, until it moves only slightly, while blood is diverted to the rest of the heart. To date, studies indicate some benefits of off-pump bypass, including a reduced need for blood transfusions and fewer cognitive difficulties commonly referred to as “pump head.” One 2001 Duke University study raised significant concerns when it found that 42 percent of on-pump bypass patients still demonstrated mental deficits five years after their bypass.
“Being on the heart-lung machine is not a natural state,” says Dr. Donald Gibson, a
According to data from the Society of Thoracic Surgeons, which tracks roughly 80 percent of
During cardiac catheterization, a physician inserts a special long, flexible tube—called an angiography catheter—into your heart and coronary arteries. Contrast media (sometimes called dye) is injected through the angiography catheter while continuous x-ray images (fluoroscopy) are taken. The dye causes areas where blood flows, including vessels and heart chambers, to temporarily become darker than the surrounding tissue. This enables the physician to see how effectively your heart is pumping, and to determine if there are any narrowed blood vessels. Blood pressure measurements are also taken at this time.
From 1979 to 2001 the number of cardiac catheterizations increased 304 percent. An estimated 1,208,000 inpatient cardiac catheterizations were performed in 2001. The average total charge for patients hospitalized for diagnostic cardiac catheterization increased from $11,232 in 1993 to $16,838 in 2000. The total number of patients increased from 626,690 to 693,472, while the average length of stay decreased from 4.7 days to 3.6 days.
Cardiac catheterization carries a slightly increased risk when compared with other heart tests. Generally the risk of serious complications ranges from 1 in 1,000 to 1 in 500. Risks of the procedure include the following:
* Exposure to ionizing radiation (causes cancer and tumors in the blood vessels)
* Cardiac arrhythmias
* Cardiac tamponade
* Trauma to the artery caused by hematoma
* Low blood pressure
* Reaction to contrast medium
* Hemorrhage
* Stroke
* Heart attack
Blue toe syndrome a condition where the feet or other body parts turn purple, almost bruised looking where cholesterol is disturbed from the procedure and has moved into the small blood veins in his feet. Clinical presentation can range from a cyanotic (blue) toe to a diffuse multi-organ systemic disease that can mimic other systemic illness. Mortality can be higher than 70% depending on the scope of the condition. This is often very painful. A possibility later on is amputation.
Considerations associated with any type of catheterization include the following:
In general, there is a risk of bleeding, infection, and pain at the IV site.
There is always a very small risk that the soft plastic catheters could actually damage the blood vessels.
Blood clots could form on the catheters and later block blood vessels elsewhere in the body.
The contrast material could damage the kidneys (particularly in patients with diabetes).
In 2002, 2,154 heart transplants were performed in the United States. There are 257 organ transplant centers in the United States, 140 of which perform heart transplants. Each year thousands more Americans would benefit from a heart transplant if more donated hearts were available. In the United States in 2002, 77 percent of heart transplant patients were male, 74 percent were white, 19 percent were ages 35-49, and 50 percent were ages 50-64. In 2002 the 1-year survival rate was 86 percent. Based on heart transplants performed from 1994 to March 2001, the 3-year survival rate was about 77 percent, and the 5-year survival rate was 71 percent.
An estimated 571,000 PTCA procedures were performed on 559,000 patients in 2001 in the United States. From 1987 to 2001 the number of procedures increased 266 percent. In 2001, 66 percent of PTCA procedures were performed on men; 51 percent were performed on people age 65 and older.
Americans are also failing to control a common cause of heart death–their blood pressure. Only 39 percent of adults with high blood pressure had their levels controlled to below 140/90 mm Hg, considered the highest desirable blood pressure, according to the National Center for Quality Assurance.
Hypertension is a major risk factor for other diseases–coronary angina pectoris (heart disease), cerebral vascular disease (stroke), heart failure (heart muscle weakness) and uremic poisoning (kidney failure). High blood pressure leads to these disabling and often fatal conditions by its effects on the structure of the arteries that carry blood from the heart to all the body organs, and by its influence on the structure and function of the heart muscle itself. Blood pressure is actually the pressure inside the arteries of the body, the force exerted by the blood against the walls of the arteries through which it flows. Just as there is water pressure inside the water pipes in your home, so there is blood pressure inside the arteries of your body. Hypertension damages the arteries and sets in motion some of the processes leading to thrombosis–narrowing of arteries for blood flow and thickening and hardening of the vessel walls. The usual cause of thrombosis is endothelial separation, or rupture of the inside lining of blood vessels from poor nutrition.
Thirty-seven million adults in this country have hypertension or high blood pressure, and this group forms the pool from which one of these potentially lethal conditions develops. High blood pressure (HBP) is defined as systolic pressure of 140 mm Hg or higher, or diastolic pressure of 90 mm Hg or higher. “Prehypertension” is systolic pressure of 120-139 mm Hg, or diastolic pressure of 80-89 mm Hg, or both. One in 5 Americans (and 1 in 4 adults) has HBP. About 22 percent of American adults or about 45 million people have “prehypertension.” Of those with HBP, 30 percent don’t know they have it; 34 percent are on medication and are controlling it; 25 percent are on medication but don’t have their HBP under control; and 11 percent aren’t on medication. A higher percentage of men than women have HBP until age 55. From ages 55-74 the percentage of women is slightly higher; after that a much higher percentage of women have HBP than men do. HBP is 2-3 times more common in women taking oral contraceptives, especially in obese and older women, than in women not taking them.
About half of people who have a first heart attack and two-thirds who have a first stroke have blood pressures higher than 160/95 mm Hg. People with systolic blood pressure of 160 mm Hg or higher and/or diastolic blood pressure of 95 mm Hg or higher have a relative risk for stroke about 4 times greater than for those with normal blood pressure. Hypertension precedes the development of congestive heart failure (CHF) in 91 percent of cases. HBP is associated with 2-3 times higher risk for developing CHF.
Beginning in the early 1960s, a group of researchers began investigating the mechanism by which mercury caused hypertension. This group demonstrated that mercury causes the smooth muscles in the walls of arteries to contract, thereby causing hypertension. Inorganic mercury causes blood vessel constriction and subsequent hypertension within minutes after exposure. Organic mercury (methylmercury, ethylmercury) did not; neither did lead–even in large quantities. None of the other metals tested (silver, copper, barium, vanadium) were nearly as effective as inorganic mercury in causing hypertension. Researchers found that larger, acute doses of inorganic mercury are so toxic to the heart muscle that severe systemic hypotension occurs. They also found that inorganic mercury causes actual pathological damage to the heart muscle tissue, and which severely decreases heart function resulting in a dramatic drop in blood pressure. High blood pressure is caused by mercury preventing the passage of calcium into the heart muscle cells, increasing the force of the heart muscle contraction.
Total mention mortality–HBP was listed as a primary or contributing cause of death in about 251,000 of over 2,400,000 U.S. deaths in 2000. From 1991 to 2001 the age-adjusted death rate from HBP increased 36.4 percent, but the actual number of deaths rose 53 percent. The 2001 overall death rate from HBP was 16.5. Death rates were 13.7 for white males, 47.8 for black males, 13.4 for white females and 38.9 for black females. As many as 30 percent of all deaths in hypertensive black men and 20 percent of all deaths in hypertensive black women may be due to HBP. In 2004 the estimated direct and indirect cost of high blood pressure is $55.5 billion.
A deficiency of vitamin E, vitamin C, vitamin A and/or missing amino acids, any or all, can lead to endothelial fragility: a tendency of the squamous epithelial (flat) cells which line the blood vessels to lose their adherent quality. Upon separation (traumatic) from normal impact of circulatory forces, endothelial interruptions are bridged with adhesive substitutes forming the foundation of thrombus (to “patch” the lesion). Since the pressure in the arteries is the pressure against which the heart must pump, high blood pressure makes the heart work harder, increases the heart muscle’s demand for oxygen, and can eventually lead to heart muscle failure. Hypertension itself rarely causes symptoms: it’s known as the “silent killer.”
Evidence suggests that some decrease in blood pressure may result from consumption of certain lactobacilli, or milks fermented with lactobacilli. Studies done with hypertensive rats have shown a positive effect. Studies with human subjects are limited. However, one study conducted with subjects with hypertension showed that a fermented milk decreased systolic blood pressure by 10-20 mm Hg. Attempts to identify the component causing the anti-hypertensive effect suggest that at least in one case it is due to a part of the bacterial cell wall. This implies that the cells need not be alive to mediate this effect. Other research demonstrated that two tripeptides generated by growth of Lactobacillus helveticus during the fermentation of milk yielded an anti-hypertensive effect. These tripeptides were shown to inhibit angiotensin converting enzyme, a key enzyme in elevating blood pressure. These results suggest that consumption of certain lactobacilli, or products made from them, may reduce blood pressure in mildly hypertensive subjects.
From the early 1970s to early 1990s, the estimated number of noninstitutionalized stroke survivors increased from 1.5 million to 2.4 million. The prevalence of TIAs in men is 2.7 percent for ages 65-69 and 3.6 percent for ages 75-79. (A TIA, or transient ischemic attack, is a mini-stroke that lasts less than 24 hours.) For women, TIA prevalence is 1.6 percent for ages 65-69 and 4.1 percent for ages 75-79. On average, every 45 seconds someone in the United States has a stroke. Each year about 700,000 people experience a new or recurrent stroke. About 500,000 of these are first attacks, and 200,000 are recurrent attacks. Each year about 40,000 more women than men have a stroke. Men’s stroke incidence rates are 1.25 times greater than women’s. The difference in incidence rates between the sexes is somewhat larger at younger ages but nonexistent at older ages. Of all strokes, 88 percent are ischemic, 9 percent are intracerebral hemorrhage, and 3 percent are subarachnoid hemorrhage. The age-adjusted stroke incidence rates (per 100,000) for first-ever strokes are 167 for white males, 138 for white females, 323 for black males and 260 for black females. Blacks have almost twice the risk of first-ever stroke compared with whites. Stroke accounted for more than 1 of every 15 deaths in the United States in 2001. About 50 percent of these deaths occurred out of hospital. Total mention mortality–about 282,000. When considered separately from other cardiovascular diseases, stroke ranks No. 3 among all causes of death, behind diseases of the heart and cancer. On average, every 3 minutes someone dies of a stroke. 8-12 percent of ischemic strokes and 37-38 percent of hemorrhagic strokes result in death within 30 days. From 1991 to 2001 the stroke death rate fell 3.4 percent, but the actual number of stroke deaths rose 7.7 percent. Because women live longer than men, more women than men die of stroke each year. Women accounted for 61.4 percent of U.S. stroke deaths in 2001.
Diabetes increases the risk of stroke, with the relative risk ranging from 1.8 to almost 6.0. Diabetes is one of the most important risk factors for stroke in women. In several studies, the impact of diabetes on stroke risk is greater in women than in men. The prevalence of diabetes increased by 8.2 percent from 2000 to 2001. Since 1990 the prevalence of those diagnosed with diabetes increased 61 percent. The age-adjusted prevalence of major CVD for women with diabetes is twice that for women without diabetes, and the age-adjusted major CVD hospital discharge rate for women with diabetes is almost four times the rate for women without diabetes. An estimated 49-69 million adults in the United States may have insulin resistance. One in four of them will develop type 2 diabetes.
Based on data from the CDC Diabetes Surveillance System, 1997-2000: In 2000 the self-reported prevalence of any CV condition was 28.8 per 100 diabetic population among persons ages 35-64, 45.7 per 100 among persons ages 65-74, and 53.5 per 100 persons age 75 and older. In 2000, among persons with diabetes age 35 and older, 37.2 percent reported being diagnosed with a CV condition, i.e., CHD, stroke or other CV condition. In 2000, among persons with diabetes age 35 and older, the age-standardized prevalence of self-reported CHD, angina or heart attack, was almost three times that of self-reported stroke (22.1 percent vs. 8.0 percent). In 2000, 4.4 million persons age 35 and older with diabetes reported being diagnosed with a CV condition. 2.9 million were diagnosed with CHD (i.e., self-reported CHD, angina or heart attack) and 1.1 million reported being diagnosed with a stroke.
Total mention mortality — 213,000. The 2001 overall death rate from diabetes was 25.3. Death rates were 26.2 for white males, 49.9 for black males, 20.5 for white females and 48.1 for black females. From two-thirds to three-fourths of people with diabetes mellitus die of some form of heart or blood vessel disease. Heart disease death rates among adults with diabetes are 2 to 4 times higher than the rates for adults without diabetes.
The cost of cardiovascular diseases and stroke in the United States in 2004 is estimated at $368.4 billion. This figure includes health expenditures (direct costs, which include the cost of physicians and other professionals, hospital and nursing home services, the cost of medications, home health care and other medical durables) and lost productivity resulting from morbidity and mortality (indirect costs). By comparison, in 2003 the estimated cost of all cancers was $189 billion ($64 billion in direct costs, $16 billion in morbidity indirect costs and $109 billion in mortality indirect costs). In 1999 the estimated cost of HIV infections was $28.9 billion ($13.4 billion direct and $15.5 billion indirect). From 1979 to 2001 the number of cardiovascular operations and procedures increased 417 percent. In 2004 the estimated direct and indirect cost of CHD is $133.2 billion. In 2001 an estimated 1,051,000 angioplasty procedures, 516,000 bypass procedures, 1,314,000 diagnostic cardiac catheterizations, 46,000 implantable defibrillators and 177,000 pacemaker procedures were performed in the United States. The majority of the cost is for inpatient hospitalization so anything that prevents the disease and complications and the need for rehospitalization can reduce cost.
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Heart disease is by far the number one killer in the United States, although a third of those deaths could be prevented if people followed better diets and exercised more, the American Heart Association said in an annual report. In the spring of 1984, Cardiovascular News interviewed Dr. William P. Castelli, medical director of the Framingham Heart Study, Framingham, Massachusetts. He stated: “For most heart attack victims, diet alone would work–if we advocated diet in American medicine, but we don’t.” Many studies show that a better diet and a little exercise can prevent many deaths, yet Americans ignore the most basic guidelines. People in poorer countries, who live on a simpler diet containing mostly grains and vegetables, and very little food of animal origin, have low cholesterol levels, and CVD is virtually unknown. Cardiovascular disease is the leading cause of death in many other societies than the United States. In Finland, which has the world’s highest milk consumption, heart disease is even higher than in the United States, which rates second per capita. Once rare or unknown, coronary heart disease is soaring in the developing world as the rich diet and life-style of the more affluent nations take hold. Traditional societies in the Middle East, Europe, Asia and elsewhere intuitively understood the relationship between personal and social health and a balanced daily diet.
In the Yellow Emperor’s Classic of Internal Medicine, the medical book of ancient China, the heart is likened to the monarch of the body who governs the other principal officials or organs: “Where the monarch is bright, the officials below him will feel secure, and when this principle is applied to nourish life, one will enjoy longevity without health hazards. When the same principle is applied to rule the world, the world’s oldest medical text recommends consumption of millet and warns that “an excessive consumption of salted foods will cause the blood vessels to become stiffened...”
Bread, or the staff of life–whole cereal grains, including brown rice, whole wheat, barley, millet, oats, rye and corn–were the cornerstone of all civilizations previous to our own. Supplemented with fresh garden vegetables, beans, sea vegetables, fermented foods, and small amounts of seasonal fruit, seeds and nuts, grains were eaten daily and formed the center of every meal. Animal food was consumed very sparingly and eaten with substantial quantities of grain and vegetables. Until modern times, when this way of eating changed, heart disease, cancer, and other degenerative illnesses were almost unknown. In 1904, the word atherosclerosis was coined to describe the hardening of the arteries. In 1912, several decades of coronary research culminated in the first clinical description of myocardial infarction in a medical journal.
In the 1920s, heart attack, the common term for this condition, became a household word. By World War I, heart disease emerged as a major ailment, accounting for about 9% of fatalities in the United States. The primary causes appear to be dietary, and they may be traced back to the change in patterns of food consumption begun during the latter part of the nineteenth century. In January 1977, the premises and goals of the natural foods movement received support in Dietary Goals for the United States, a report issued by the Senate Select Committee on Nutrition and Human needs. Headed by former presidential candidate George McGovern and vice-presidential nominee Robert Dole, the committee took testimony and held hearings on the nation’s health. The final document concluded: “During this century, the composition of the average diet in the United States has changed radically. Complex carbohydrate–fruit, vegetables and grain products–that were the mainstay of the diet, now play a minority role. At the same time, fat and sugar consumption have risen to the point where these two dietary elements alone now comprise at least 60% of total calorie intake, up from 50% in the early 1900s. These and other changes in the diet amount to a wave of malnutrition–of both over- and under-consumption–that may be as profoundly damaging to the Nation’s health as the widespread contagious diseases of the early part of this century.
The over-consumption of fat, generally, and saturated fat in particular, as well as refined sugar, refined salt and alcohol have been related to six of the leading causes of death: heart disease, cancer, cerebrovascular diseases, diabetes, arteriosclerosis, and cirrhosis of the liver.” After more than a generation of neglect, the Senate report opened the door to nutritional common sense in this country. There had been earlier studies linking diet and degenerative disease, but these had made little impact on the medical profession and rarely received publicity. Through the mid-1970s, many physicians continued to ignore dietary considerations, and heart patients in coronary care units were served meals including steak, fried potatoes, ice cream and other foods high in fat or sugar. Despite organized opposition from the meat and dairy food lobbies, Dietary Goals for the United States was well received by a great number of readers, nutritionists and educational and consumer organizations and sent shock waves through the food industry, the medical profession, public school lunch programs, and other segments of society responsible for providing basic nutrition. During recent years, at least 37 international health organizations and task forces on cardiovascular disease have issued similar recommendations. These organizations include the International Association of Cardiology, Intersociety Commission on Heart Disease Resources, World Health Organization, Canadian Department of National Health and Welfare, American Heart Association, Royal College of Physicians and British Cardiac Society, Australian National Heart Foundation, West German Federal Health Office, and Netherlands Nutritional Council.
Mercury is a strong metabolic poison: it can harm any living cell or process. Although mercury is found in many forms, they all work the same way once they get into the body and reach the cells. The toxic potential of the various forms depends on their ability to enter the body. The most toxic forms of mercury, namely mercury vapor and methylmercury, easily enter the body and penetrate its cells. Inhaled mercury vapor, from amalgam dental fillings, travels rapidly and dramatically to heart tissue. This type of mercury exposure presents a far greater risk to the heart than does mercury derived from fish (organic mercury) or medications (inorganic mercury). For more than 70 years, scientific evidence, has demonstrated widespread cardiovascular effects from inorganic mercury and mercury vapor. Recent published studies have revealed that subjects with amalgam fillings experience significant mercury exposure to the tissues of the cardiovascular system and have significantly higher blood pressure, lower heart rate, lower hemoglobin levels, and lower percentages of red blood cells. They also have a greater incidence of impaired cardiac electrical and neurotransmitter function, pathological changes in heart muscle tissue, damage to blood vessels and heart valves, arrhythmias, constriction of coronary arteries, chest pains, rapid heart beat, anemia, increased potential for blood clots, fatigue, tire easily, and are tired in the morning.
These studies have demonstrated how mercury poisoning from inhaled mercury vapor from dental amalgam fillings affects the cardiovascular system. Damage by mercury occurs when it attaches to or enters the cells of the body; no matter what form the mercury is in when it enters the body. Ethylmercury and methylmercury are very toxic forms of mercury because they easily enter the body and its cells. Mercury vapor is also very toxic for the same reason. Medical knowledge about cardiovascular disease was minimal prior to the twentieth century. In the mid-19th century, the effect of occupational exposure to mercury in workers in mirror factories and the use of mercury in the treatment of syphilis was undertaken. In 1861, it was reported that the activity of the involuntary muscles are affected.
Together with a weakness of the voluntary muscles, there is generally an impairment of the heart. The pulse is slower, with greater lability; resting heart rate was 60-70 beats/minute, but at the slightest agitation, the rate rapidly rose to 80-100. Sometimes pronounced tachycardia occurred. In the 1930s, it was recognized that mercury caused damage to the heart and blood vessels. It was then discovered that mercury poisoning had a paralyzing influence of heart and circulation, followed by a reduction in blood pressure and death. In 1938, researchers found serious vascular damage from mercury exposure. The analysis of cardiovascular disease is dependent upon sophisticated testing and sophisticated research, neither of which was available until the 20th century. Because of these factors, the cardiovascular effects of exposure to mercury were not recognized until fairly recently. Medical scientific researchers began investigating mercury accumulations in cardiovascular tissue of humans and animals in controlled experiments in the 1950s.
The animals exposed to mercury vapor had much higher levels of mercury in the heart and brain, as well as larger amounts in the thyroid, adrenals, spinal ganglia and nerves, testes, and ovaries. Exposure to mercury vapor results in much larger accumulations of mercury in the heart than does exposure to inorganic mercury. The mercury levels in the heart were three to four times those found in the brain of exposed animals, after only one hour of exposure. In humans, exposure to mercury vapor results in a high and rapid accumulation of mercury in heart tissue. Levels of inorganic mercury, methylmercury, and total mercury accumulation were measured and significantly high levels of mercury were found in heart tissue, about the same amounts as were found in the brain. It was also found that the levels of inorganic mercury in the heart increased with age, while the levels of methylmercury decreased. In human autopsy studies, high levels of mercury were found in the pituitary glands of dental personnel and in subjects with amalgams.
Mercury absorbed from dental amalgam is rapidly taken up by the heart tissue, in even greater amounts and more rapidly than that which is absorbed into the brain. Mercury specifically derived from dental amalgam fillings also influence heart function by accumulating in the brain, pituitary, thyroid, and adrenals, and are also target organs after exposure to mercury vapor. Among the earliest widespread indications of the cardiovascular effects of mercury were in victims of Acrodynia, a disease syndrome known to be caused by mercury, and was diagnosed primarily in children who were being exposed to various mercury compounds, mostly a mercurous chloride compound called Calomel, which was commonly used as a teething powder and to combat “diaper rash.” In 1952, it was found that Calomel (mercurous chloride) enhanced the influence of epinephrine (adrenaline) in constricting arteries and causing high blood pressure and tachychardia in children.
Mercury’s toxic action on a wide range of tissues, including those in the cardiovascular system, is scientifically proven. Researchers have found that mercury affects several aspects of cardiac function, including the ability of heart muscle to contract, the electrical conduction activity in the heart, and the function of regulators of cardiac activity. Mercury toxic subjects exhibited an increased occurrence of rapid heart beat, irregular pulse, chest pains, heart palpitations, and high blood pressure. Mercury blocks the action of acetylcholine, the neurotransmitter that passes the nerve impulse from the vagus nerve to the heart muscle. Both acetylcholine and the nerve receptors in the heart muscle contain thiol (sulfur/hydrogen) proteins. When mercury attaches to the thiol protein in the heart muscle receptors and in the acetylcholine, the heart muscle can’t receive the vagus nerve electrical impulse for contraction.
Mercury accumulates in the heart muscle and heart valves, causing damage by attaching to thiol (SH-) or sulfhydryl (sulfur/hydrogen combination) proteins. This damage is indicated by EKG changes and confirmed by histologic study. The damage is found in the coronary arteries and capillaries supplying blood to the heart tissue and in the heart muscle itself. Mercury has a high affinity for and readily binds to the mineral selenium in living tissues. The higher the affinity (attraction) between chemicals or elements, the stronger they bond to each other, and the harder it is to separate them. The thiol combination is extremely common in the human body. It occurs as part of certain amino acids, which are the building blocks of proteins. Since these amino acids are used to build cells, hormones, and enzymes, the occurrence of the thiol combination in the body is not only common but extremely important, as normal function is altered. There are several thiol locations in the hemoglobin molecule in the red blood cells used to transport oxygen throughout the body. Mercury accumulates in red blood cells in humans and other animals.
When this mercury attaches to the thiol sites, the hemoglobin can’t carry as much oxygen as it should. This results in decreased availability of oxygen which is needed by all body cells, and explains one way that mercury toxicity can cause chronic fatigue symptoms. This same interference occurs wherever thiols occur in the body, including the cardiovascular system. Mercury and other thiol poisons affect several aspects of cardiac activity, such as the response to regulating nerves (especially the vagus nerve) and chemicals, the electrical activity of the heart, and the ability of the heart muscle to contract.
Heart muscle consists of two major proteins, actin and myosin. The function of muscle tissue depends on the interaction between these two proteins and their combination to form actomyosin, resulting in tissue contraction. The connection of these two proteins occurs at thiol sites in the myosin molecule. If mercury attaches to those thiol sites, the muscle tissue will not be able to function. With mercury vapor intoxication, there is a decreased activity of respiratory enzymes and sarcoplasmic ATPase.
Cell respiration consists of a series of chemical reactions that provide the needed energy for cell functions. Cell respiratory enzymes are very sensitive to mercury; it alters or inhibits their function by removing the hydrogen atom from the thiol group. Mercury affects heart function by influencing hormones from the pituitary gland (pituitrin). Pituitrin contains several active hormones that have a profound and important influence of the body, including one that affects the constriction of arteries. Chronic mercury exposure affects cardiovascular functioning by interfering with cardiovascular regulating hormones (dopamine, epinephrine, and norepinephrine). In test animals, mercury exposure increases the force of heart muscle contraction, causing high blood pressure, by blocking the passage of calcium ions into the heart muscle cells. Low concentrations of various mercury compounds accelerate blood coagulation (clotting) process. Unborn babies are highly exposed to and susceptible from their mothers’ dental amalgam fillings.
Prenatal exposure to mercury produces marked toxicity to babies, including a hi