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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 BC). 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 US 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.
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 hypertension and an increased left ventricle requirement to 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, rock-like 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 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 long-standing 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 (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 US labor force, accounting for 19 percent of disability allowances by the Social Security Administration.
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. Dietitians 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 “essential” 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 for 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 kidneys 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 remnants 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, Kurashik 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.