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Heart Disease

HEART HEALTH PRODUCTS

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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.

Cardiovascular Disease

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.”

Blood Flow

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.

Blood Viscosity

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.

Bypass Surgery

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

Bypassing the 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 Houston heart surgeon who has performed more than 1,500 off-pump bypasses. “We’re seeing that, as patients become more educated, they come to us and say, “If I have to have this bypass, I would prefer to have it off-pump,” says Gibson, who operates in a team with Dr. Miguel Gomez at Memorial Hermann Heart & Vascular Institute—Memorial City. But Gibson remains in the surgical minority.

According to data from the Society of Thoracic Surgeons, which tracks roughly 80 percent of U.S. coronary artery bypass grafting procedures, just 20.4 percent of more than 141,000 heart bypasses in 2004 were performed off pump. A study, published in 2004 in the Journal of the American Medical Association, involved nearly 200 bypass surgeries performed by an Emory University surgeon experienced in off-pump bypass. The study, which randomly assigned patients to on-pump or off-pump, found that blood flow through the grafts was similar at one year. The number of deaths was also similar with one patient in the beating heart group dying within 30 days and two patients in the on-pump group.

Cardiac Catheterization

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).

Heart Transplants

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.

Percutaneous Transluminal Coronary Angioplasty (PTCA)

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.

Hypertension

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.”

Probiotics

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.

Stroke

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 Mellitus

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.

Costs

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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Diet

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’s Effects on the Heart

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 high incidence of abnormal hearts, characterized by dilation of the heart with a thinning and weakening of the heart walls. Inhaled mercury vapor penetrates the placental membrane far more thoroughly than does inorganic mercury, thereby greatly increasing the potential for this fetal damage. The integrity and proper function of living cells depends on the ability of certain materials to pass into and out of the cells. The cell membrane contains a great many thiol sites. Mercury binds to these sites and prevents the passage of certain materials into and out of the cells. Mercury blocks the enzyme in the cell membrane that actively passes calcium in and out of the muscle cells by attaching to the thiol part of the enzyme. Calcium is necessary for the proper function of heart muscle.

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. It takes time for chronic mercury exposure to cause enough damage to result in a clinically detectable dysfunction. This is a predominant characteristic of heart disease. It takes the body 30-70 days to eliminate one half of each dose of mercury. If a person is only exposed to very small doses of mercury vapor, but is exposed many times each day, the mercury will slowly build up in body tissues. Some time may elapse before enough mercury builds up in heart tissue to cause noticeable symptoms.

In 1964, investigators conducted electrocardiogram tests on victims of organic mercury poisoning in Iraq in 1960. A serious outbreak of mercury poisoning, including many deaths, resulted from farmers’ families eating organic mercury-treated grain intended for planting. All victims demonstrated EKG changes, denoting damage to the heart. Cardiac arrhythmias, abnormal beats of the ventricles, and paroxysmal ventricular tachycardia were also found. These changes were attributed to mercury damage to the heart’s pacemaker, (sinoatrial node), the electrical conduction system of the heart, and reduced blood supply to the heart muscle (myocardial ischemia). In 1977 researchers found that the pathology found in mercury poisoning is a result of damage to the blood vessels and subsequent blood supply. Nerve damage resulted from reduced blood flow. They found a thickening of arteries in the victims and hardening of the blood vessels in the brain and other arteries in the body, as well as thrombus (clot) formation is in the blood vessels. The victims also demonstrated high blood pressure, damage to heart muscle, and heart attacks. They also showed damage to the Islets of Langerhans in the pancreas, the cells that produce insulin.

Varicose Veins

Varicose veins are veins that have become swollen and overly relaxed and are visible and sometimes bulging on the surface of the skin. They are a result of weakened walls of the veins along with a sluggish blood flow.

Hemorrhoids

Hemorrhoids, often called piles are round, purplish protuberances at the anus and, in effect, are varicose veins of the rectum. They are swollen veins in the mucous membrane inside or just outside the rectum.

Tinnitis

Tinnitis is another condition that can, in many instances, be a result of varicosity or fragility of the tiny capillaries in the ear. When persons complaining of hearing noises that are not from the environment. Such noises can be a result of hardening and loss of elasticity and weakening of the walls of the small arteries in the ear. Even some types of migraine headaches are related to blood vessels that are weakened and too dilated, allowing rushes of excess blood to the head.

Obesity

Forty percent of Americans are fat and getting fatter. Thirty-four million Americans are obese. The chance of sudden death from heart attack is more than three times as great for subjects who are 20% overweight. Approximately 115 million persons in America are overweight, even though not categorized as obese. The Average dietary fat consumption has increased by 31% and carbohydrate consumption has increased by 43% since 1910.

Each year an estimated 300,000 U.S. adults die of causes related to obesity. Obesity profoundly affects life span. An estimated 8,830,000 children and adolescents ages 6-19 are considered overweight or obese, based on the 95th percentile of body mass index (BMI) values in the 2000 CDC growth chart for the United States. Based on data from NHANES IV (1999-2000), the prevalence of overweight in children ages 6-11 increased from 4.2 percent to 15.3 percent compared with data from 1963-65. The prevalence of overweight in adolescents ages 12-19 increased from 4.6 percent to 15.5 percent. Over 10 percent of preschool children between the ages of 2 and 5 are overweight, up from 7 percent in 1994.

Obesity rates are significantly higher among people with disabilities, especially blacks and those ages 45-64. The prevalence of obesity (BMI 30 or higher) in 2001 increased 5.6 percent between 2000 and 2001. Since 1991 the prevalence of those who are obese increased 75 percent.

A 20-year-old white male with a BMI greater than 45 is estimated to have 13 years of life lost (YLL) due to obesity. A 20-year-old white woman with a BMI greater than 45 is estimated to have 8 YLL due to obesity. For black men the estimate is 20 YLL and for black women the estimate is 5 YLL. Nationally, the estimated annual cost attributable to obesity-related diseases is about $100 billion. Among children and adolescents, annual hospital costs related to obesity were $127 million during 1997-99.

Obesity is serious. Fat on the belly means fat on the heart and fat clogged arteries. One pound of fat requires one mile of blood vessels to nourish the cells, resulting in an enormous increase in the workload of the heart. Greenland Eskimos, living on their traditional diet high in meat and fats, and also high in cholesterol, are free of CVD, as well as cancer, diabetes, arthritis and other degenerative disease. The fatty acids in fish oils are the secret of the Eskimos’ good health on their traditional diets. Actually, there are many groups to be found around the world who do not kill themselves on cholesterol-rich food the way we do.

Also Eskimos do not drink fluoridated water. Fluoride consumption can result in calcification of the arteries...better known as hardening of the arteries or arteriosclerosis. Fluoride has long been known to be part of the ‘limestone rock’, which deposits on the walls of the blood vessels. It has also been known for a long time that, in soft tissues, the highest concentration of fluoride is found in the aorta.

Fitness

The following data are based on leisure-time physical activity. Note: “Vigorous activity” is defined as activity causing sweating and hard breathing for at least 20 minutes on 3 or more of the 7 days. “Moderate activity” is defined as activities such as walking or bicycling lasting for at least 30 minutes on 5 or more of the 7 days. 54.6 percent of Americans age 18 and older are not active enough to meet physical activity recommendations. 38.3 percent of Americans age 18 or older report no physical activity. 61.7 percent engage in at least some physical activity. 22.7 percent engage in light-moderate physical activity at least 5 times per week. People who are college-educated, in higher income brackets or living in the West have a higher prevalence of recommended activity. Married women are more likely than women in any other marital status group to engage in at least some physical activity.

31.3 percent of U.S. adults age 18 and older engage in regular leisure-time activity. For age groups 18-24 and 25-64, women are less likely than men to engage in regular leisure-time physical activity. The relative risk of CHD associated with physical inactivity ranges from 1.5 to 2.4, an increase in risk comparable to that observed for high blood cholesterol, high blood pressure or cigarette smoking. 51.7 percent of high school students were enrolled in physical education classes in 2001, but only 32.2 percent attended classes daily. 61.5 percent of children ages 9-13 don’t participate in any organized physical activity (PA) during their nonschool hours and that 22.6 percent don’t engage in any free-time PA. By the age of 16 or 17, 31 percent of white girls and 56 percent of black girls report no habitual leisure-time activity. Lower levels of parental education are associated with greater decline in activity for white girls at both younger and older ages. For black girls, this association is seen only at the older ages. Cigarette smoking is associated with decline in activity among white girls. Pregnancy is associated with decline in activity among black girls but not among white girls. A higher BMI is associated with greater decline in activity among girls of both races.

Physical inactivity is more prevalent among women than men, among blacks and Hispanics than whites, among older than younger adults and among the less affluent than the more affluent. A recent study of over 72,000 female nurses indicates that moderate-intensity physical activity such as walking is associated with a substantial reduction in risk of total and ischemic stroke. Many people believe that exercise and general fitness, in itself, will provide optimum health. The fact is however, that fitness and health are two separate and distinct phenomena. Fitness is a measure of how much physical activity you can do. It is a reflection of your functional capacity, your ability to perform physical work. In scientific or physiologic terms, it is measured by the maximum amount of oxygen your body can use when you are performing at your peak effort. Health, on the other hand, is a reflection of the presence or absence of disease, or your vulnerability to it. You may be free of disease, and relatively resistant to the important maladies of our time, yet be incapable of much physical activity because you are simply physically unfit. Conversely, you can be very physically fit, trained to a high level of physical fitness, and yet be so unhealthy as to be at risk of imminent death. The elements of fitness are only measures of mechanical efficiency, not health of the cardiovascular system.

The so-called cardiovascular training effect, the most widely used gauge of cardiovascular fitness, is only a measure of mechanical efficiency of the system, not of its health. Two examples may illustrate the point: The late James Fixx, a runner who is correctly credited with being one of the prime moving forces in the early years of the “exercise revolution” that has swept across this country, took up running as a means of preventing cardiovascular disease. He became extremely fit, and ran several miles with ease almost every day. Yet, despite his high level of fitness, he fell dead while running at the age of 52, a victim of severe coronary heart disease. The first astronaut to walk in space, Edward H. White, was selected for this unique endeavor by meeting several criteria, including an extremely high level of physical fitness.

Every measure of fitness used, indicated the highest degree. It was assumed, of course, that his cardiovascular health was equally excellent. Yet, when he died in a tragic fire not too long after his space walk, autopsy study showed that he had severe and widespread coronary heart disease. Many studies have demonstrated that the lymphatic pump mechanism functions at the maximum during physical activity. Conversely, when a person is at rest or asleep, the lymphatic pump is working the least amount with a resultant decrease in lymph flow. In turn, when one sleeps longer than necessary, tissue spaces will tend to become congested with protein and carbon dioxide...the reason for the puffy appearance upon arising and mental sluggishness from excess CO2. Obviously, then, regular exercise is not only of benefit in staying alert and healthy...it is most essential, (if feasible), for maintaining normal capillary dynamics toward support of tissue repair mechanisms...the basic requisite for overcoming a good number of diseases. For many, exercise is more important than diet. Moderate, regular exercise does not increase the appetite and it burns up extra calories.

Homocysteine

Homocysteine is a natural substance made by the body. Homocysteine functions at a metabolic crossroad that can affect all the methyl and sulfur group metabolism of key enzymes, hormones, and vital nutrients. Many people lack the ability to break it down completely and high homocysteine levels usually occur because of a buildup in the system due to the inability to clear homocysteine because of faulty methionine pathways (mercury and lead toxicity). When it is not completely broken down, it becomes a very dangerous substance that can exert harmful effects and increase disease-causing oxidation. When it is broken down completely, it can furnish necessary substances for other beneficial reactions in the body (methyl and sulfur groups). These necessary substances provide the fuel for vital processes like liver detoxification, adrenal gland support, neurotransmitter synthesis, and joint cartilage and bone regeneration. Homocysteine is a very dangerous substance that is harmful to arteries, which makes it a risk factor for heart disease if it is not broken down completely. Homocysteine can cause clotting, increase harmful oxidation, and can injure the blood vessel wall (especially if already weakened by x-rays), allowing cholesterol and fat to infiltrate into the wall and cause what is known as a foam cell. This foam cell swells and protrudes into the space of the artery and obstructs the blood trying to flow past, potentially resulting in a heart attack. The artery is usually damaged and cholesterol is oxidized before infiltration into an artery and creation of a foam cell can occur, and homocysteine can damage the artery, oxidize the cholesterol, and decrease circulation, all of which favor heart disease.

The first correlation with homocysteine and disease involved cardiovascular disease, but since then, toxic effects have been revealed on other organ systems, including the liver, adrenals, joints, nerves, and general system blood vessels, including placental tearing. Neuropsychiatric conditions have been traced to homocysteine problems, and a correctly functioning pathway is vital to neurotransmitter synthesis. Other conditions which have been linked to high homocysteine levels include: neural tube defects, multiple sclerosis, rheumatoid arthritis, spontaneous abortion, placental abruption, renal failure, osteoporosis, and type II diabetes. Homocysteine is not toxic when the pathway is functioning properly. Synergistic nutrients facilitate the pathway, prevent toxic levels of homocysteine from accumulating, and make it possible for a functioning pathway to provide necessary methyl groups and sulfur groups for a myriad of biochemical reactions, especially those needed for detoxification and joint and cartilage repair.

There are nutrients which facilitate the methionine pathway and reduce homocysteine levels. These include: betaine, dimethylglycine, and vitamins B₆, B₁₂, folic acid, niacinamide, choline, magnesium, and molybdenum. Homocysteine is recycled to methionine in the presence of B₁₂, folic acid, and methyl donors such as choline or betaine (trimethylglycine). Vitamin B₆ (pyridoxyl-5-phosphate is the active form of B₆) and magnesium help convert homocysteine to cysteine.

Molybdenum is an essential trace mineral necessary to convert the toxic sulfite molecule to the important sulfate molecule, needed for many biochemical reactions. Niacinamide, a B vitamin, can increase the activity of two crucial enzymes which are needed to facilitate conversion of homocysteine to non-toxic substances. Niacinamide is also necessary for steroid hormone synthesis (cortisol, estrogen, progesterone, testosterone, DHEA), and when chronic stress on the adrenals favors cortisol production, a limitation in niacinamide and/or precursors allows cortisol to be made at the expense of other steroid hormones (such as DHEA). This results in increasingly large ratios of cortisol to DHEA. This can lead to tissue insensitivity to insulin. In turn, all the excess cortisol will need to be conjugated (detoxified in the liver), and this process happens largely through sulfur-dependent detoxification pathways in the liver. For this to happen, the homocysteine path has to be functioning correctly to provide the sulfur groups for liver detoxification, providing these sulfur groups can take some of the stress of the adrenals when excess cortisol is present. Zinc, selenium and magnesium are all minerals which are important cofactors in enzyme reactions of the homocysteine pathway.

Zinc and selenium are cofactors for antioxidant enzymes. Magnesium is needed to take methionine to SAM (S-adenosylmethionine), and for the end reaction which takes the toxic sulfite to the essential sulfate, and for glucose metabolism (glucose is a substrate for glucuronic acid, hyaluronic acid, N-acetyl glucosamine, and chondroitin sulfate, which are all building blocks for cartilage and joint repair). Chronic mercury inhalation from mercury amalgam dental fillings, with mercury’s great affinity to bind to methionine and cysteine, has the potential to decrease the availability of these amino acids and affect the metabolism of both vitamin B₁₂ and folate.

Nutrition

Although it is important to be physically fit and to have adequate relaxation, it is equally important to get adequate nutrition from eating proper food. The underlying cause of all degenerative disease is toxemia and malnutrition. Refined sugars, refined oils, and refined starches are all deficient in minerals and vitamins. Our slightly salty bloodstream is a replica of the ancient sea in which life developed during most of its biological history, and each cell is surrounded by fluid similar in composition to seawater. The blood consists of liquid in the form of plasma and of formed elements consisting of red blood cells, white blood cells, and platelets. Several dozen other nutrients and compounds also circulate in the bloodstream, including fat, cholesterol, glucose, sodium, potassium and urea. The transport of oxygen and nutrients in the blood is essential for life, and the efficiency with which it is accomplished is essential for life, and the efficiency with which it is accomplished directly influences our health and well-being. Diet is the principal determinant of the blood’s relative acidity or alkalinity. Whole sprouted grains, raw vegetables, sprouted beans, and sea vegetables are the most balanced foods and produce strong, healthy blood that is neither too acid nor too alkaline. Through the network of capillaries, this strong blood–neither too thick nor too thin–is distributed to the cells and tissues of the body, including the brain cells, creating harmonious day-to-day health, a bright outlook, and vitality. Dr. Alexis Carrel, (Who’s Who), in his great experiment, kept the cells of an embryo chicken heart alive and in health for over 30 years by complete nutrition and complete elimination.

The normal life-span of a chicken is 7.5 to 8 years. The experiment proved that cells do not just die; they are poisoned and/or starved by the fluid that they float in. This knowledge is not new but has been with us for some time. Back in 1921, Howe, a dental researcher, found that vitamin B deficit resulted in atrophy of the parathyroid glands. Also, cramps and convulsions of Beriberi are from lowered serum Calcium and possibly secondary to loss of calcium/phosphorus balance, which is controlled by the parathyroid function. In the heart, as in all cells it is well established that the calcium ion (Ca⁺⁺) controls many biochemical processes, such as muscle contraction, cell division and neurotransmitter activation/deactivation. In the mitochondria (power plant of the cell), Ca⁺⁺ speeds up cellular respiration (production of ATP).

Ca⁺⁺ stimulates the enzyme that activates pyruvate dehydrogenase (PDH) that speeds the conversion of pyruvate into acetyl coenzyme A–the currency for the Krebs energy cycle. Ca⁺⁺ also inhibits the enzyme that inactivates the same PDH. What the heart drug digitalis really does, in a pharmacologic and/or biochemical sense, is raise the level of intracellular calcium in the heart muscle cells. This is done indirectly by chemical inhibition of the sodium-potassium pump of the myocardial cell membrane, which forces the mitochondria to inject calcium into the cytosol (cell fluid). With increased calcium in the cytosol, the contractile strength of myofibril (muscle cells) is enhanced.

Calcium is not only a regulator of functions, but essential to normal ventricular capacity for blood expulsion. From a regulatory standpoint, calcium is intertwined with other ions; potassium, sodium and magnesium. Fluctuations of sodium and potassium control the opening and closing of cell membrane calcium channels. If opened, the influx of calcium changes the plasma membrane’s electrical nature, making the membrane more resistant to depolarization. In turn, it is easy to visualize that calcium can, and does, affect blood pressure. When there is a deficiency of ionized calcium or the physiological inability to diffuse ionized calcium from the vascular system into the tissues, the left ventricular contraction loses its vigor before the end of the contractile effort. Thus, less than the intended volume of blood is pumped into the aorta and the amount of blood falling back from the aortic arch is insufficient in quantity to snap shut the aortic valve, as would be expected and is detected as a diminished or absent second sound on the phonocardiograph.

It is well established that ionized calcium will restore the ventricular contraction in many instances, that is, unless the person is deficient in unsaturated fatty acids–essential to the diffusion of ionized calcium into the tissue spaces. Also, administration of properly prepared tincture of hawthorne berries, motherwort, red clover, ginger, and cayenne pepper has been shown to alter phonocardiographic tracings toward normal, within ten minutes. The natural B-complex (nutritional yeast) is composed of two groups of vitamin elements that differ both in their solubility and in their physiological effects. The B-group is alcohol and water soluble and includes the vasoconstrictor elements necessary for normal nerve action including B₁ and its synergists, B₁₂, Pantothenic Acid and Adenine, especially B₄. The G-group is not soluble in absolute alcohol; it includes the vasodilators B₂, B₃, B₆, Choline, Betaine, Inositol, Folic Acid, Biotin and PABA, which have anti-spasmodic, and lipocaic effects.

Biochemical researcher, C.W. Carter, reported in the Biochemical Journal, 24:1811, 1930, that pigeon heart block can be cured by the administration of whole wheat, but not with vitamins B₁, B₂ or the fat soluble concentrates. Later in the text Biochemistry, 28:933-939, 1934, Carter concludes that a wheat germ constituent other than B₁ leads to complete restoration of cardiac function in pigeon heart block. Angina pectoris is as specific a deficiency condition as scurvy. All of these conditions will show a shorter than normal rest period on a heart graph. Alleviation of pain are usually experienced in 5 to 10 minutes. The graph will not return to normal for about two weeks and upwards of continuous nutritional treatment. Vitamin B₄ prevents nerve paralysis or loss of conduction power–fibrillation is the final result of this deficiency. Vitamin B₄ is a key factor in preventing heart dilation or enlargement.

This distorts the heart valves, and causes leakage (regurgitation) as exhibited by murmurs. As soon as the heart contracts to normal, the leakage stops. Utilizing a natural, complex vitamin B containing vitamin B₄ from cereal germ (refined out in grain processing), the conditions of impaired nerve transmission discussed above, can be dramatically improved and demonstrated on humans within minutes using the Phonocardiograph or Endocardiograph. No results will be seen with synthetic vitamin B-complex. Extra systoles, fibrillation and heart block are situations where nerve conduction has been impaired (heart block, bundle branch block, atrial fibrillations, atrial flutter, arrhythmia, enlargement & bradycardia). Vitamin B-complex (B₄ in particular) is required in this case. Often the arrythmia disappears within 15 minutes of the administration of a small amount of this complex.

Regurgitation and the consequent murmurs due to valvular impairment are usually due to some degree of enlargement, since the changes in position by reason of the enlargement are often the cause. The natural B-complex usually produces an immediate improvement in the muscular tone with progressive contraction of the heart towards its normal size. The disappearance or reduction of the murmur is evidence of the change. Congenital murmurs have been controlled by the use of the B-complex. Vitamin G-Complex is the protein-linked group of the B-vitamin family. It is the “original B vitamin” and has been found to be comprised of a number of different vitamins, frequently called the “B₂ complex.” Among these are riboflavin and niacinamide–these form parts of complex enzyme systems concerned with hydrogen transport in the living cell. It has the opposite effect of thiamine (B₁) and its synergists in that it relaxes muscular tissue, with particular effect on the coronary arteries, probably by its activation of the adrenal functions (tones up most arteries, but relaxes the coronaries). G-complex contains nerve relaxing factors and is usually indicated for the high strung, hypertensive, jumpy patient who has the exact opposite heart picture of the one that is B-complex deficient (shorter than normal rest period instead of the abnormally long one of a heart block). G-complex relaxes, the B-complex contracts or creates muscle tone.

VItamin E is necessary to maintain the integrity of the endothelial cells. When the protective vitamin E is not present, the chromosomes disintegrate and liquefy. Raw wheat germ is the best source for Vitamin E. Vitamin E deficiency has been associated with vascular obstructions, leg ulcers, and development of blood clots in the vascular system, phlebitis, hemorrhages into the skin and other afflictions of the blood vessels. Complex E₂, which is noted for its nitroglycerine action, is usually used in combination with G-complex because of their joint action in the same type of heart picture. Both vitamins G and E₂ are vaso-dilators and are the nutritional factors indicated in coronary thrombosis, coronary insufficiency, angina pectoris or any other vascular constriction.

In vitamin E₂ complex deficiency, the tissue demand for oxygen may rise 250%. It is important to prevent such a load from being imposed on any heart, much less a weakened and diseased one. Vitamin E deficiency specifically causes necrosis of heart muscle fibers. It is easy to see how vitamin E deficiency results in sudden death, the heart muscle is undermined and the load is increased at the same time. Adequate Selenium is required to produce the necessary Coenzyme Q required for a healthy heart. Selenium is the trace-mineral precursor to natural vitamin E complex. Selenium deficit is a factor in Endemic Cardiomyopathy called “Keshan disease.” Selenium is the most important nutrient in the control of Coenzyme Q levels. Coenzyme Q is essential to the electron transport system, coupled to oxidative phosphorylation (krebs cycle) so essential to heart muscle tone and contractile strength. It is an aid in certain energy-producing enzymatic reactions and is indispensable to heart function...the normal heart is higher in Coenzyme Q content than most other tissues. Selenium reduces myocardial damage after heart attacks and reduces heart pain. The nervous control of the heart is affected by means of a balance of power of the two divisions of the autonomic nervous system–a result of the opposing stimuli received from the sympathetic and parasympathetic (vagus) enervation.

The sympathetic enervation tends to speed up and increase the circulation of blood in response to physiological demands; the vagus inhibits according to similar demands (the former is the accelerator; the latter the brake). Where a potassium deficiency is present, there may be tachycardia (increased heart rate) due to reduced effect of the vagus, which depends on potassium for its normal tone. The patient has a laboring, fast heart that fails to calm down as it should when there is no need for its hyperactivity, as when the patient tries to sleep thus causing hypertension. The vagus (parasympathetic) system normally is the inhibitor, reducing the visceral activity when it should, as part of the autonomic system. Without blood potassium, the normal autonomic control of the heart is lost, it is an “engine without a governor,” and may race to destruction. This heart racing has been attributed to hyperinsulinism, but it is purely potassium deficiency. Potassium, administered as the organic mineral fraction of green vegetable juices, affords immediate relief (within twenty minutes). The slowing effect in this case is similar to digitalis, but is a physiological instead of a pharmacological effect.

Potassium is absorbed from the blood by stowing away sugar after heavy carbohydrate meals and this brings on heart laboring and tachycardia. Sugar is stored as phosphagen (instead of as glycogen). Phosphagen is di-potassium creatine hexose phosphate, a compound that is as loaded with energy as gunpowder for those who do little work and don’t burn up their calories regularly. Normal metabolism releases the potassium into the blood again as the sugar is consumed, ready for the next mealtime load of sugar, but, if the potassium intake is limited, the shortage can result in the serious state described above. Too much phosphagen seems to make the human body as combustible as flash-powder, cases are on record of spontaneous combustion of living victims. Victims of this reaction should eliminate from their diet, all sugar and sugar products. Where the vagus is not opposed and becomes dominant, by reason of partial paralysis of the sympathetic system, the common cause is phosphorus and phosphate deficiency. Whole grains are a great source. With vitamin deficiency to starve the endocrines and mineral deficiency to paralyze either or both divisions of the autonomic system, any combination of the two lists of consequences of autonomic unbalance is possible.

Chlorophyll and its associated fat soluble factors as found in green vegetable sources are important in cardiovascular states. Vitamins A, E, and K are all present. One of the most significant and interesting influence is in the lowering of blood pressure and strengthening the heart in arteriosclerosis. Chlorophyll is very effective in controlling pain. This effect is due to the fact that chlorophyll destroys guanidine on contact, guanidine being a toxin released by burns, trauma, or muscle fatigue. Guanidine precipitates calcium from blood serum, and is suspected to be a cause of calcification of coronary arteries, diffusing in from the muscle. Wheat grass juice, spirulina plankton, or any green leafy vegetables are good sources of chlorophyll. Where there are evidences of venous enlargement, ecchymoses and telengiectases (facial “road maps”), this deficiency may be suspected, and when these outward lesions are visible, the condition of the more irritable intestinal tract can be imagined. Colitis is especially aggravated by deficiency of chlorophyll and Vitamin K.

Vitamin K is an integral part of the vitamin C complex, and promotes the production of prothrombin, a substance essential to the formation of the fibers of fibrin for blood clotting and connective tissue to build better vascular walls: its deficiency is evidenced by vascular breakdown. Telengiectases are looked upon as indications of liver disease, rightly enough, for thrombin is made by the liver, and K deficiency causes the liver damage, no doubt, before these secondary evidences appear. Chlorophyll contributes to the control of cholesterol metabolism, like the factor in Vitamin A-complex. Varicose veins no doubt are also subject to aggravation from the same deficiency, if not a definite end result of it. Vitamin A contributes to the health of the flat cells, which line the blood vessels (endothelial cells). Cod liver oil is a good source of Vitamin A. Lack of sufficient vitamin A can result in degenerative changes in the structures of the blood vessels, slow healing and susceptibility to and loss of resistance to insult or injury. Naturally occurring Vitamin C-complex (not ascorbic acid) is absolutely necessary to blood cells and blood vessels as well. Its functions include regeneration of blood cells and maintenance of proper blood-clotting time. Some results of deficiency include degeneration of blood vessels–fragility, hemorrhages, tendency to bruise easily, varicosities, etc. Vitamin C aids in weaving cells more tightly together, obviously essential to keep blood vessels from distending. Blood vessels contain much protein, like collagen and elastin.

Vitamin C has a protein protecting and building effect; it forms colloidal intercellular substances–the protein between cells–the collagen of fibrous tissue in the blood vessels, and other “cement” substances needed to hold structures together. Lack of the Vitamin C-complex reduces the oxygen capacity of the red cells, necessitating a greatly increased volume of blood to maintain a normal oxygen supply to the tissues. In Vitamin C deficiency, the heart has more work to do. When the pulmonary circulation becomes engorged and hypertensive, this condition is associated with hypoadrenia (weak adrenals). Vitamin C complex is known to support adrenal activity. Cayenne pepper is a good source of real Vitamin C. The most important part of the C complex is tyrosinase, (organic copper) which is essential to all muscle, and the heart muscle in particular, which undergoes atrophy with replacement fibrosis in case of a lack of enough of this element. Where the heart shows a greatly increased contraction time, indicating an overworked (incompetent) muscle, natural Vitamin C-complex, containing tyrosinase (organic copper, affords a spectacular change–both in the cardiogram as well as in the disappearance of the “shortness of breath” sensation.

The P-fraction of the vitamin C-complex (rutin and bioflavonoids) is also a synergist of thrombin formation, for it may earmark calcium for thrombin deposition. The vitamin P portion of the Vitamin C-complex, in particular, is a factor in aiding the maintenance of normal blood calcium, necessary to cellular adherence. Vitamin P reinforces the walls of blood vessels. It is known to assist in clearing up vascular hemorrhagic conditions and even has been indicated for use in migraine-type headaches caused by weakened capillary walls where capillary damage permits proteins from the blood serum to leak into the cerebrospinal fluid.

Coenzymes such as Thiamine Pyrophosphate (from B₁), flavin adenine dinucleotide (from B₆), are absolutely demanded for intracellular metabolism and mitochondrial utilization of adenosine triphosphate (ATP) precursors. Without biotin (vitamin H), the coenzyme biocytin cannot be synthesized, and a lack of that particular coenzyme impairs the transfer of carbon dioxide from the cell into the circulation. Excess CO₂ in the cytosol would change intracellular pH (hydrogen ion concentration), partially inhibiting anaerobic glycolysis and reducing aerobic metabolism. The strength factor of the blood vessels is the fibrous muscular constituents. These require protein for the collagen and elastin, which support the integrity and elasticity of the blood vessel.

Each heart muscle cell is composed of eighteen different amino acids. All the amino acids are needed, but especially the sulfur-containing amino acids. Six of those eighteen amino acids (phenylalanine, lysine, threonine, histidine, tryptophane, methionine) are heat labile meaning that when a certain amount of heat is applied (as in cooking), these particular amino acids are first denatured (unraveled) and then coagulated to an insoluble state in which they cannot be utilized by the body in the formation of polypeptide chains needed for cellular repair or replacement. Even the denaturation involves structural changes in the protein molecule, which results in a loss of species specificity. The denaturation alters viscosity, surface tension and replicative utilization of biologically active proteins, which includes hemoglobins, myoglobins and enzymes as well. Digestive enzymes attack denatured proteins much differently than undenatured proteins, and coagulation renders the protein irreversibly insoluble. So a source of raw protein with all the natural amino acids is helpful...properly balanced and readily available to the cells. It has been said that cooking protein foods destroys four-fifths of the protein value. Heat, acids, trypsin and hydrolysis all cleave polypeptide chains, which make up enzymes–the functional units of cellular metabolism.

As a result, some of the amino acids are denatured or lose their characteristic folding and the important catalytic activity is lost. So cooking of protein foods, prior to ingestion, can denature or unfold some of the amino acids required for cellular enzyme biosynthesis. A deficit of iron, copper, zinc, magnesium, manganese, potassium, nickel, molybdenum or selenium, impairs enzymatic production and or function. Besides being made up of eighteen amino acids, the heart muscle cell is rich in myoglobin and the enzymes of the Kreb’s citric acid cycle plus the electron transport system, from which the cardiac muscle cell obtains constantly needed, contractile energy from adenosine triphosphate (ATP) utilizing acetoacetate, lactate and fatty acids–where glucose is completely oxidized to CO₂ and H₂O. Because of its “energy-rich” phosphate bonds, ATP releases molecular energy upon muscle fiber receptors for muscle work. The Krebs cycle uses B₃ (NAD) five times, B₁ (TPP) two times, Pantothenic acid two times and Biotin three times. B₁ or its coenzyme factor thiamine pyrophosphate (TPP) is required to decarboxylate pyruvic acid. Coenzyme A uses or incorporates pantothenic acid. When pantothenic acid is deficient, acetic acid is not properly reduced. Biotin, normally synthesized in the intestine is needed to transport CO₂ from the cell into the circulation. Heavy metal toxicity blocks biotin function, while antibiotics stop or restrict biotin production in the intestinal tract.

In the anaerobic phase of glycolysis, fluoride blocks the very important enolase reaction, which impairs glucose metabolism. In the final stage, the passage of the hydrogen electron particles derived from pyruvate into the electron transport system, is also dependent upon certain nutrients. Of importance is, again nicotinamide adenine dinucleotide (NAD) requiring vitamin B₃, along with iron, copper, phosphate, potassium, magnesium and calcium (Ca2⁺). Zinc (Zn2⁺) is present in many NAD and NADP-linked enzymes. Selenium is an essential component of glutathione peroxidase which functions to protect cells from H₂O₂ damage. Carnitine is an amine (nitrogen-containing organic compound) synthesized in the liver from the amino acid lysine, which as you saw above is coagulated and denatured by heat. It is most important that the diet be 1% Lysine...the requirement of this protein fraction is greater than any of the other amino acids. Carnitine is an extractive from both liver and muscle. Carnitine transports acyl-CoA into the mitochondrion inside of the cells. A deficiency of Carnitine impairs fatty acid (beta) oxidation and triglycerides accumulate in the muscle cytoplasm. Thus, carnitine deficiency is characterized by progressive muscle weakness (loss of low intensity-prolonged work efficiency), essential to cardiac muscle–along with abnormal lipid storage in the muscle.

Vitamin F (essential fatty acids) is a usual constituent of vitamins A and E. Vitamin F acts as a catalyst to bring about oxygen transfers to muscle cells, thus providing the muscle action needed for contraction of the blood vessels. These essential fatty acids are also necessary to keep calcium in proper solution in between the endothelial cells of the blood vessels so that the cells ‘stick together’ and do not separate, resulting in varicosity. Vitamin F deficiency has been related to hemorrhagic spots on the skin and swelling of the extremities. Magnesium phosphate is a form of the mineral magnesium and is also essential for the proper tone of blood vessels. A deficit of Magnesium phosphate (or an impaired nerve supply) can permit an abnormal relaxation of the blood vessel walls with the result of a dilatation or varicosity. The Collinsonia plant (stone root) has been utilized in any condition where the vascular system has lost its tone and the blood vessels have been enlarged, as in varicose veins or hemorrhoids for example.

Thyroid

Hypothyroidism is a major factor in cardiovascular disease. Credit for realizing that thyroid deficiency is one of the most potent factors in causing heart attacks must go to the pathologists of Vienna about 1890. They did not appreciate the significance of their discovery since heart attacks had not been described as yet; they could hardly claim credit for curing a disease that did not exist. Pathologists soon noted that after total thyroidectomy, autopsies revealed an exaggerated hardening of the arteries. Without normal thyroid function, no organ of the body works efficiently, especially the heart. The over- or under-production of thyroid hormones will affect overall body function. Both the pituitary and the thyroid display an affinity for accumulating mercury.

Organic mercury causes severe damage to both the endocrine and neural systems. Studies have documented that mercury causes hypothyroidism, damage of thyroid RNA, autoimmune thyroiditis (inflammation of the thyroid), and impairment of conversion of thyroid T4 hormone to the active T3 form. Large percentages of women have elevated levels of antithyroglobulin (anti-TG) or antithyroid peroxidase antibody (anti-TP).

Mercury blocks thyroid hormone production by occupying iodine binding sites and inhibiting hormone action even when the measured thyroid levels appears to be in the proper range. Mercury can have a negative effect on both iodine and thyroid status. The enzymatic effects of mercury intoxication can be overcome by the administration of thyroid hormone thyroxine. Through a feedback loop, the pituitary releases thyrotropin-releasing hormone (TSH), which in effect tells the thyroid how much thyroxine hormone to release into the blood. Mercury first stimulates and then suppresses the thyroid function. Chronic intake of mercury for more than ninety days results in signs of mercury poisoning, together with decreased uptake of iodine and depression of thyroid hormonal secretion. The thyroid gland has four binding sites for iodine. When mercury attaches to one of these sites, the hormone activity is altered. There is a relationship to thyroid function and the nutritional status of folate, vitamin B₁₂, and methionine.

There is also a strong association of lowered zinc intake and lowered basal metabolic rate, and lowered thyroid hormones and lowered protein utilization. Mercury affects the nutritional status of folate, vitamin B₁₂, methionine, and zinc, as well as protein. The thyroid gland is controlled by the pituitary gland. A person may have adequate levels of T3 and T4 hormones, but if the hormones are contaminated, for practical purposes the person is functionally thyroid deficient. Thyroid imbalances play a major role in chronic heart conditions such as clogged arteries and chronic heart failure. A report by von Eilsberg in 1895 clearly showed that removal of the thyroid from the sheep or goat would produce arterial degeneration in arteries throughout the animal including the coronary vessels supplying the heart. It was animals that eat only plants–that were chosen for the experiment and these animals never eat cholesterol-containing foods.

Cholesterol is not found in the plant world. This early experiment clearly demonstrated that thyroid deficiency, and not dietary cholesterol, was implicated in arterial degeneration whose characteristics were similar to those in the human. With Hyperthyroidism or excessive thyroid hormone production, the metabolic rate is increased–the cardiac output, being proportional, is increased, so heart rate and blood pressure are likewise elevated. More oxygen is used and more CO₂ is produced, so blood must travel through the lungs more often. Excessive thyroid hormone causes prolonged work for the heart, eventually decreasing myocardial strength. There is a greater demand for vitamin A and other vitamins since hyperthyroidism may create a deficit. The thyroid hormone activates and increases vitamin requirements. The result of hyperthyroidism is a person who is very weak and tired; in some cases, exhausted. The excessive rate of breakdown of protein eventually weakens the muscle cells.

Hypothyroidism is a lack of proper thyroid hormone secretion–leading to a reduction in the basal metabolism of 50% or more. CO₂ production is decreased, as is oxygen consumption. A decrease in cell energy results in lowered heat production–the body temperature is lower and the person feels cold all the time. Hypothyroid persons “burn” foods or fuel more slowly, so, along with the reduced utilization of oxygen, there is a resultant decreased call for an active circulation. Respiration may be slower, heartbeat is slowed, and its stroke volume falls below normal. There is poor muscle tone, pronounced asthenia (loss of strength), slowed relaxation/contraction ratio, and great susceptibility to fatigue. Most often body weight increases and obesity can result even though appetite may not be increased. Carbohydrate metabolism is affected, including reduced cellular uptake of glucose (with resultant fatigue), reduced hydrolysis of glucose by enzymes (glycolysis) and reduced formation of glycogen from fats rather than carbohydrates.

Since thyroxine accelerates the beta-oxidation of free fatty acids in the cell mitochondria, a reduction of the thyroid hormone in hypothyroidism would increase serum cholesterol, triglycerides and phospholipids. The body requires vitamin F (essential unsaturated fatty acids) to metabolize iodine to nourish the thyroid. A deficiency of vitamin F brings about a lowering of the blood iodine level, and as vitamin F is supplied, the blood iodine immediately rises. So, persons with low blood iodine might find vitamin F to be more important than iodine itself. The thyroid lowers blood cholesterol, but if vitamin F is not available in sufficient amounts, the thyroid secretions could become toxic. In numerous other tests (Turner in 1938, Anitschkow’s work of 1913, as well as Friedland’s in 1927), suggested that it was the thyroid deficiency, which was responsible for the damage and not the cholesterol itself. Thus, years before the rapid rise in heart attacks, cholesterol was exonerated as the culprit, and thyroid deficiency was firmly established as the cause of atherosclerosis. Many patients with low basal metabolic rates have elevated serum cholesterol. Low thyroid function even in an infant can start the pathological damage to the blood vessels by depositing the mucopolysaccharides in the walls of the arteries. They are always present in atherosclerosis and most other pathological states.

They are combinations of complex proteins with one of the sugars in the molecule. The thyroid controls other fats in the blood as well as the cholesterol. To some, serum cholesterol levels are used as a diagnostic indicator for thyroid function. Although there are two conditions, both rare and easily ruled out, that may elevate cholesterol and not be from a weak thyroid. One is nephrosis, a condition in which large quantities of protein are lost in the urine. Since much of this protein must be manufactured in the liver, this may interfere with the elimination of cholesterol by that organ. Liver damage may also be associated with an elevated cholesterol since the excretory process is retarded.

In hypothyroidism there is a reduction in blood-flow through all the organs including the kidneys. Atherosclerosis in the kidney artery could further reduce the blood flow–creating hypertension, which is very common in hypothyroidism. Thyroid therapy usually relieves elevated blood pressures seen in the general practices of aware physicians. Young individuals can develop severe, incapacitating heart disease as a result of thyroid deficiency and this disease is readily amenable to nutritional thyroid support. Vitamins A, B, C, D, E and F are all concerned in the maintenance of a normal thyroid function. Vitamin B complex and specifically Vitamin B1 are especially important to the treatment and proper function of the thyroid. The restorative action of vitamin B₁ is due partly to the fact that it normalizes fat absorption and lipoid economy. High blood cholesterol generally follows glandular atrophy and inhibition that takes place from the use of refined foods, with damage to the thymus, adrenals, sex glands and thyroid. Decreasing the intake of animal products, and replacing them with foods from plant sources lowers cholesterol levels.

A strict vegetarian diet increases the vitamin, mineral and essential fatty acid content, and also lowers the fat intake. Two quarts of milk per day can raise the cholesterol level from 180mg/dl to 400 mg/dl in less than 2 months. Milk is low in several vitamins, minerals and essential fatty acids. Excess body fat increases blood cholesterol levels and CVD. Losing weight lowers the risk and the cholesterol level. Excess refined sugars, refined starches (white flour, white rice, pastas), and refined or altered fats and oils raise cholesterol levels. Returning to natural complex, high fiber carbohydrates and natural, unrefined fats and oils lower cholesterol. Smoking raises cholesterol level and CVD. So does coffee. Quitting reverses the trend.

Alcohol

While some recent findings indicate that people who “have a few” every day live longer and have fewer heart attacks, a growing body of scientific evidence shows the detrimental effects of alcohol on human health far outweigh any potential benefits. Alcohol abuse carries severe penalties in terms of coronary mortality. In fact, heavy drinkers have been shown consistently to have the highest risks of coronary heart disease. Research has established two harmful ways in which alcohol affects the heart and cardiovascular system. The first is blood pressure–the elevated blood pressure caused by drinking has made alcohol a primary culprit in the cause of hemorrhagic stroke, particularly intracerebral hemorrhages, which are the most lethal kind of stroke. Another way in which alcohol promotes heart disease is in its effect on the heart muscle itself. It seems to be a metabolic toxin, depressing the heart’s muscular function, causing irregular heartbeat, or arrhythmia, and may even cause cardiomyopathy, a deterioration of heart muscle, over a prolonged period–leading to the need for a heart transplant. Alcohol allows sodium and calcium to accumulate in cells. If this goes on long enough, it can actually dissolve the cell. An abnormal amount of sodium and calcium in the heart cells interferes with the rhythm of the heartbeat as well as the heart’s contraction.

Phosphorus deficiency is another observable consequence of regular alcohol intake and can occur even in moderate drinkers. Alcohol not only leaches phosphorus from the cells, but also acts as a kind of poison that prevents even dietary supplements of phosphorus from curing the deficiency–this can lead to cardiomyopathy. Heavy alcohol drinking interferes with the brain’s supply of oxygen. In a phenomenon known as “blood-sludging,” red blood cells clump into wads that block capillaries and keep out oxygen. Alcohol is a major cause of such clumping. The neurons normally fed by the capillaries quickly die if those pathways are plugged. Alcohol is the second leading avoidable cause of all deaths in the U.S.

Caffeine

America is the world’s largest coffee consumer, and current statistics show that what used to be “good to the last drop” isn’t good for you at all. The average cup of coffee contains 150 milligrams of caffeine. Teas generally contain more caffeine than does coffee, except for herbal teas. The amount of caffeine in just one cup of coffee (150 mg.) is a lethal dose if injected into the bloodstream! Caffeine does more than keep you awake. Caffeine is linked with a host of human ills, from irritability to high blood pressure. After just one cup of coffee, respiration increases up 13%, metabolism rises as much as 25%, and heartbeat jumps 15%. Caffeine not only increases heartbeat, in large amounts it causes an irregular beat. In animals, caffeine produces alterations in the blood vessels similar to changes produced by prolonged resentment and anxiety. This kind of stress is closely linked to high blood pressure, a major factor in heart attacks and strokes. Caffeine also boosts the blood’s level of fatty acids, which contribute to high blood pressure as they build up on artery walls. Caffeine makes dangerous inroads on other parts of the body, too. Its far-reaching effects are explained by the fact that it invades every organ and tissue in the body.

About 99% of the caffeine you consume goes to work within 15 to 45 minutes. And once it is in your system it is there for some time. The half-life of caffeine can range from 2½ to 7½ hours. It can take up to 30 hours for 97% of ingested caffeine to clear out of the bloodstream. If you remove it from your diet, traces may remain for a week. Caffeine’s effects are more pronounced in some people than in others; as you age, you’re likely to grow more sensitive. It causes deficiencies in essential vitamins, especially some of the important B vitamins. Coffee and tea acidify the pH of the body, robbing alkaline minerals that are used for buffering the acids.

Smoking

About a quarter of all Americans smoke cigarettes, which cause an estimated one in five deaths from cardiovascular diseases, according to the American Heart Association said. Its report said 37,000 to 40,000 non-smokers die from heart disease every year because of exposure to secondhand cigarette smoke. Since 1965 smoking in the United States has declined by over 40 percent among people age 18 and older. In 2001, 38.5 percent of male students in grades 9-12 and 29.5 percent of female students reported current tobacco use; 22.1 percent of males and 8.5 percent of females reported current cigar use; and 14.8 percent of males and 1.9 percent of females reported current smokeless tobacco use. In 1996 about 15 million children and adolescents under age 18 were exposed to environmental tobacco smoke in the home. About 80 percent of people who use tobacco begin before age 18. The most common age of initiation is 14 to 15.

About 5 million American men and women use chewing tobacco. The prevalence varies widely by region and sociodemographic factors. Rates are highest in the South and rural areas. Men use chewing tobacco at 10 times the rate for women. Use rates increase as years of education decrease for both men and women. Among Americans age 18 and older, 25.2 percent of men and 20.7 percent of women are smokers, putting them at increased risk of heart attack and stroke. Smoking prevalence is higher among those with 9-11 years of education (35.4 percent) compared with those with more than 16 years of education (11.6 percent). It’s highest among persons living below the poverty level (33.3 percent) compared with other income groups. 47.7 percent of working adults age 17 and older who don’t use tobacco report exposure to environmental tobacco smoke at home or at work. 37.4 percent of nonsmoking adults are exposed to environmental tobacco smoke at home or at work. From 61.3 percent to 82.1 percent of adults report that their workplace has a smoke-free policy. According to the World Health Organization (WHO), one year after quitting, the risk of CHD decreases by 50 percent. Within 15 years, the relative risk of dying from CHD for an ex-smoker approaches that of a long-time (lifetime) nonsmoker.

An estimated 3.2 million Americans tried their first cigarette this year; most of these new users (2.3 million) were ages 12 to 17. An estimated 1.7 million Americans began smoking cigarettes daily in this year. More than half of these new smokers were younger than age 18. This translates to more than 4,000 new regular smokers per day, including more than 2,000 youths. After increasing since the early 1990s, the number of 12- to 17-year-olds initiating daily smoking dropped significantly between 1997 and 1998, from 1.1 million in 1997 to 864,000 in 1998.

From 1995 to 1999 an average of 442,398 Americans died each year of smoking-related illnesses. 33.5 percent of these deaths were cardiovascular-related. About 35,000 nonsmokers die from CHD each year as a result of exposure to environmental tobacco smoke. The risk of death from CHD increases by up to 30 percent among those exposed to environmental tobacco smoke at home or work. Smoking costs Americans over $157 billion annually in health-related economic costs. This estimate includes adult smoking-attributable productivity costs and medical expenditures, and smoking-attributable neonatal medical expenditures.

Giving up smoking seems to be the one most positive step that can be taken toward cardiac health and good health in general. Most people do not know of the vascular damage from smoking that results in thousands of leg amputations each year. Smokers have a 70% greater rate of death from all causes than non-smokers. Smoking is the second most severe risk factor in heart disease (after high blood pressure). Smokers in the U.S. have a three-times greater chance of dying from heart disease than from lung cancer and it is believed that the risk of stroke for smokers is 50% higher than for non-smokers. Women who use oral contraceptives and also smoke increase their heart attack risk as much as 20 times. Nicotine is so lethal that if you ingested the nicotine from five cigarettes, you would die within three minutes. A smoker consuming one pack per day will ingest almost 10 grams of nicotine and 125 grams of tar per year.

Cigarette smoking is now as important a cause of death as were the great epidemics in Europe since the fifteenth century and all known epidemics of yellow fever in history. Smoking just one cigarette also increases the pulse an extra 15 to 25 beats per minute, lasting up to 20 minutes after the last puff. For the average smoker, that’s more than 10,000 extra beats per day for their heart. At the same time blood pressure is increased 10 to 20 points (mm/Hg). Inhaling nicotine from just one or two cigarettes blocks nerve impulses that forces the smooth muscles of the small blood vessels to constrict, this leads to increased resistance to blood flow and increases blood pressure while simultaneously raising the heart rate.

This effect lasts from 15 to 20 minutes, just long enough to light up another cigarette. Smoking just one cigarette constricts peripheral vascular lumen size (artery opening size) in humans to one-fourth of its normal area, nearly doubling the artery wall thickness and reducing the artery’s elasticity by more than 50%. All smokers know that their “wind” is affected by their smoking. This occurs when muscle action slows because of insufficient oxygen. The reserve they miss in muscle action could save their life if a clot in one of the coronary arteries reduced the blood to their heart. The bad effects of smoking are increased by carbon monoxide and hydrogen cyanide, which interferes with the blood’s oxygen delivery. The hemoglobin molecules in the red blood cells, will bind with carbon monoxide and hydrogen cyanide. In fact, the chemical affinity of hemoglobin for these substances is 300 times greater than it’s affinity for oxygen, reducing the oxygen-carrying capacity up to as much as 15%.

Carbon monoxide (CO) also contributes to heart disease and lung disorders and results in changes in the blood vessels that may lead to hardening of the arteries. Carbon monoxide has long been recognized as a dangerous gas. It is present in concentrations of 1% to 5% of the gaseous phase of cigarette smoke. The amount of carbon monoxide produced increases as the cigarette burns down. Carboxyhemoglobin levels in smokers vary from 2% to 15% depending on the amount smoked; degree of inhalation, and the time elapsed since smoking the last cigarette. Oxygen is essential for cellular activities and even a slight decrease can impair all bodily functions. An inactive smoker is twice as likely to die from their first heart attack as an active smoker, and nine times as likely to die from their first heart attack as an active non-smoker. The more active you are, the better your chances, whether you smoke or not.

Sitting next to a smoker, a non-smoker can be exposed to carbon monoxide levels more than twice as high as the maximum set for industry exposure. When non-smokers leave a smoky environment, it takes hours for the carbon monoxide to leave their bodies. Unlike oxygen, which is breathed in and then out again as carbon dioxide within minutes, CO in the blood lasts for hours. Tobacco smoke also contains cadmium, which, besides being a toxic metal, raises the blood pressure. More cadmium can enter the body from cigarette smoke (1.5 mcg/pack) than from the diet and drinking water. The impact of smoking on the heart and blood vessels is reversible. Studies have shown that ex-smokers can cut their risk of heart disease in half in just two years, and their chances of having a fatal heart attack are no greater than those of non-smokers in 10 to 15 years. Atherosclerosis can be reversed. The body can repair itself, if given the materials it needs to do so. Pritikin, using dietary changes and exercise, a low-calorie, low-fat, high-complex carbohydrate diet and walking rehabilitated many cases of severe arterial disease. The food we eat is converted into energy by the body; it is needed for physical activities and for the continuous process of growth, repair and regeneration of tissue.

Dairy Products

Milk fat also contains a substance called xanthine oxidase (XO). Since more oxygen is needed to carry hemoglobin to cells enveloped with mucous, the amount of oxygen available to the brain decreases, and dairy food contributes to uneven thinking, dulled reactions and emotional dependency. Homogenization allows XO to pass into the bloodstream intact. When foreign XO enters the bloodstream, it creates havoc by attacking specific targets within artery walls. The specific target within the arteries is called plasmalogen, a tissue making up 30% of human heart muscle and artery wall cells. Plasmologen’s presence is vital for the integrity of the outer cell membrane analogous to the way mortar holds bricks together in a wall. The direct attacks cause lesions within artery walls and the body’s protective mechanisms respond to the damage by scarring and laying down calcified plaques.

The simple thickening and hardening of the arteries is known as arteriosclerosis, whereas atherosclerosis is characterized by the additional accumulation of cholesterol (not dietary) and fatty deposits laid down adjacent to scars and plaques. Gradually, the artery wall thickens, obstructing the flow of blood. Arteries lose their elasticity in later stages of the disease and additional calcium is deposited. Calcification can contribute to high blood pressure which is actually not a disease in itself. High blood pressure is merely a symptom. The process of XO damage actually starts in the mother’s womb. Mother’s milk contains about 4.4% fats, of which an average of 8% is the essential linoleic acid (LA). It also contains gamma-linolenic acid (LNA) and traces of dihomogammalinolenic acid (DGLA)–both of which are intermediates in the production of the different members of the prostaglandin family. Mother’s milk, by ensuring the newborn of a plentiful supply of prostaglandins, gives the baby a healthy cardiovascular start into its new world. The cholesterol content of dairy products, combined with the sticky fatty acids creates a burden for the body that has to be carried by the fat-dispersing essential fatty acids, which must come from another source. Human milk, although it also contains cholesterol, also contains the dispersing essential fatty acids, which help to keep cholesterol from settling in the walls of our arteries.

Fiber

Fiber, a long-neglected food, has become a significant nutritional discovery and a valuable necessity in the everyday diet. Fiber is the part of the food that you don’t digest; you eat it and you eliminate it. Fiber holds water, and thus provides bulk that moves food easily and quickly through the digestive tract, keeping the passages open. Fiber is a subclass of carbohydrate that consists of nonstarch polysaccharides and lignin, and its major constituents are cellulose, hemicellulose, lignin and pectins, which are not broken down during passage through the gastrointestinal tract and are excreted in the stool. Although fiber itself does not supply nutrients per se, fiber has now moved to the position of being an essential nutrient, the deficiency of which seems to have serious consequences. Lack of dietary fiber produces low fecal bulk, which in turn has been found to cause or contribute to coronary artery disease, high cholesterol and high blood pressure, among other disorders. Wheat or oat brans are a palatable, wholesome and inexpensive source of dietary fiber that can be added to the everyday diet for good health.

X-rays

In his latest (1999) book, Radiation from Medical Procedures in the Pathogenesis of Cancer and Ischemic Heart Disease: Dose-Response Studies with Physicians per 100,000 Population, Dr. John Gofman, Professor Emeritus of Molecular and Cell Biology at the University of California, Berkeley, and a member of the faculty at the University of California Medical School at San Francisco, presents strong evidence that medical radiation is a major cause of cancer and of atherosclerosis (coronary heart disease). By medical radiation, Dr. Gofman is referring mainly to X-rays, including fluoroscopy and CT (CAT) scans. The mechanism is simple to state: Radiation causes genetic mutations that eventually give rise to disease. Gofman is not saying that medical radiation is necessarily the only cause of cancer and coronary heart disease. He does not mean that cancer is not caused by smoking, poor diet, genetic inheritance, pesticides, diesel exhaust, dioxin and toxic chemicals encountered on the job. Cancer and heart disease both have multiple causes. For cancer (or an atherosclerotic plaque) to develop, a cell must undergo several separate gene mutations. Most occur from exposure to gene-damaging substances in the environment. Gofman is not opposed to medical X-rays. Rather, he is opposed to unnecessary exposure from X-rays. He and others have shown over the years that medical X-ray exposures in the U.S. could be cut by at least 50% with no loss of medical information. The careful use of modern X-ray equipment and techniques can reduce X-ray exposure by half (or more) without sacrificing any medical benefits. Thus, at least half the cancers caused by medical X-rays are completely unnecessary.

Dr. Gofman calculates that in 1993, 50% of all cancers in women and 74% of all cancers in men were attributable to X-rays. About 500,000 people die of cancer each year in the US. If 60% of these deaths are attributable to X-rays and half are unnecessary, we are talking about 150,000 unnecessary cancer deaths each year in the U.S. Gofman calculates that the proportion of coronary heart disease (CHD) attributable to X-rays is slightly higher than the proportion of cancers. Among men in 1993, 63% of CHD deaths were attributable to X-rays, and 78% among women. So, in rough numbers, 70% of CHD deaths are attributable to X-rays, Gofman believes. Since CHD caused roughly 460,000 deaths in the U.S. in 1993, then, if Gofman is right, 70% (or 322,000) of these deaths are attributable to X-rays and half of these (or 161,000) are unnecessary. He found disease statistics for the entire U.S. population, broken down into nine census districts (1940 to 1990 for cancer, and 1950 to 1990 for coronary heart disease). Then he correlated these disease statistics, year by year, to the number of physicians per 100,000 population in each of the nine census districts. The density of physicians per 100,000 population provides a relative measure of the medical radiation per 100,000 population in the nine districts by year.

Gofman has shown that cancer death rates rise in lock-step with increasing density of physicians in a census district, while non-cancer deaths decline in lock-step with increasing density of physicians per 100,000 population, except in the case of coronary heart disease which follows the rising pattern of cancer. Thus, Gofman’s hypothesis, that CHD is linked to medical radiation, “fell out of the data.”

Because he had decades of experience researching the causes of CHD (he has written three books on heart disease), and because he knows the radiation literature so well, Gofman was able to put two and two together: Radiation induces mutations in the coronary arteries, giving rise to what he calls dysfunctional clones (mini-tumors) in the smooth muscle lining the arteries. Using his “physician density” method, Gofman estimates that medical radiation caused 83% of female breast cancer in the US in 1993. Using a completely different method, Gofman estimated in 1995 that medical radiation was responsible for 75% of US breast cancer. The two estimates, by two completely different methods, are remarkably similar.

Radiation Pellets

The ignorance of modern cardiology is vast. Medical researchers are now headed down a bizarre path that subjects trusting heart patients to high-dose gamma radiation pellets in their arteries! High-dose beta radiation, delivered along with balloon angioplasty or stenting, using intracoronary beta radiation in the treatment of lesions and re-stenosis (re-narrowing of an artery). Cardiologists and heart surgeons are confronted with serious after effects in their patients due to conventional treatments. Re-stenosis (plaque growth) caused by smooth muscle cell proliferation, is common after heart surgery and angioplasty.

Neointimal hyperplasia, is a common response to injury of the vessel wall during angioplasty. The American Heart Association estimates that the coronary arteries re-occlude after surgery in 40% of the patients under the care of cardiologists. Re-stenosis remains a major clinical challenge in interventional cardiology today. The new “high-tech” way around this problem is to use dose-dependent radiation to interfere with or perhaps destroy the ability of the intima to heal itself. Several FDA sanctioned studies are now actively investigating whether intra-arterial radiation (as pellets or “seeds”) improves the success rate of coronary by-pass operations and angioplasty. From the increasing level of mass desensitization (television news reports) it can be surmised that this procedure will soon be sanctioned by the FDA.

The radiotherapy system consists of a source wire, a source delivery unit and a centering catheter. The source wire is flexible and incorporates a radioactive isotope into its tip. The delivery unit stores the source wire when it is not in use and automatically advances and retracts it during a procedure. The source wire is advanced through the centering catheter, which is placed across the area to be treated. Has modern medicine lost its collective mind? According to John Gofman, medical radiation causes the lesions in the first place. Then they want to add more radiation to take away the natural ability to heal! Medicine has metamorphed into the antithesis of healing. It is incomprehensible that any doctor would willingly interfere with the natural healing process simply to make their lucrative surgeries more attractive. High-dose intra-arterial radiation treatments are absurd, inhumane, cruel, and nullify any chance for a nutriton-based therapy to succeed. Cardiologists are willing to subject heart patients to a treatment that is more cruel and unusual than punishment our laws permit for criminals. The proposed use of “high-dose” radiation particles inside arterises to stop the regrowth of plaque, caused by open-heart surgery and angioplasty/stent procedures, is at best unethical, and at worst criminal. To the extent intra-arterial radiation treatments interfere with the ability of the artery to heal normally, these radiation treatments make success from nutritional approaches impossible. Radiation would interfere with any non-invasibe therapy that relies on healing. Early MDs/scientists recognized that plaque formation is uniform and localized.

Most surgically removed plaque is within inches of the human heart where the blood vessels are stretched and bent, implicating high blood pressures and mechanical stress caused by the heart beat. It is now generally accepted that atherosclerotic plaques deposit in response to injury. The 1985 Nobel Prize was awarded for the discovery of the lysine binding sites. The Unified Theory, relying on the Nobel Prize, and earlier work, blames mechanical stress fractures (caused by high blood pressures, stretching and bending, etc.) for the lesion. It is unlikely that the primary cause of the lesions that lead to heart disease are caused by “poisons” circulating in the blood, because plaques are not randomly distributed ( A typical heart bypass uses plaque-free veins from the leg.).

According to theory, the root cause of atherosclerotic plaque deposits is a vitamin C deficiency. This deficiency limits our ability to produce the structural super-protein collagen. Heart disease is unknown in most animal species. Humans are less resistant to damage from the heart beat’s mechanical stress than animals because they lack vitamin C (not ascorbic acid) deficiency, a deficiency impossible in most animals! Humans must supplement 100 times the RDA of vitamin C to get an equivalent of what animals generally make in their livers or kidneys.

The correct terminology for cardiovascular disease is either “chronic” scurvey or “sub-clinical” scurvey. Medicine has been deliberately steered astray about vitamin C since the 1940s. Elevated cholesterol, elevated homocysteine, and oxidized cholesterol then, are effects, not the cause of CVD. Sugar intake is more closely correlated to cardiovascular disease than cholesterol intake. Pauling and Rath claim that specific non-toxic substances, called Lp(a) binding inhibitors, taken orally will prevent and even dissolve existing atherosclerotic plaque build-ups. The three primary Lp(a) binding inhibitor substances are vitamin C, lysine and proline. They increase blood concentrations of important substances that will strengthen and heal blood vessels, lower Lp(a) blood levels, and keep Lp(a) levels low, and inhibit the binding of Lp(a) molecules to the walls of blood vessels. Lysine and proline work to unbind Lp(a) from the arterial wall. Unlike ordinary drugs, there are no health risks. There is an awesome elegance that these binding inhibitors are completely non-toxic, yet they have been shown to dissolve plaqe in vitro. They are also the basic building blocks of collagen. The theory places poor collagen production at the root of the heart disease problem. Since plaque formation is a surrogate healing process, doctors should not be surprised that plaque reoccurs after invasive surgery.

Mainstream medical science has known since 1989 that only Lp(a) (not LDL cholesterol) binds to form atherosclerotic plaques. Lp(a) is an evolutionary surrogate for low vitamin C in humans. Not only will high dose intra-arterial radiation interfere with the healing of chronic scurvy, the great risk nuclear cardiologists subject these patients to is completely unnecessary. Patients who are subjected to radiation will not be able to heal normally, and they will likely suffer premature death. If the patients live, how can anyone know the dangerous side effects that radiation may itself cause. Since radiation is being widely studied, it is evident that cardiovascular doctors, as a group, are entirely ignorant of the nutritional approach or the Linus Pauling unified theory. Why are some of the most educated individuals in our society the most ignorant about the condition they are supposed to treat on a daily basis?

No profit-oriented drug company will inform cardiologists about the unified theory or dietary approach. So how does the average nuclear cardiologist learn about it? They don’t! No cardiologist or heart surgeon has ever been informed or heard about vitamin B, vitamin E, essential fatty acids, antioxidants, vitamin C and lysine from an official source or respected authority. They do not realize that they can completely cure their patients in less than six months, simply, safely, and with the good effects becoming pronounced after as little as two weeks. Ignorance perpetuates itself. Cardiologists cannot believe this could be true and that they could not know. But this information was first made available to the world in the 1940s, by Linus Pauling.

Cardiologists routinely tell their patients that there is no value in nutritional therapy. The doctors who use radiation to stop re-stenosis do not really understand the disease they are charged to treat. If they do understand, then they are acting in a criminal manner. The conclusion is, therefore, that the true nature of heart disease is unknown to cardiologists who should otherwise know that re-stenosis is completely preventable and that high-dose radiation procedures actually cause lesions and are completely unnecessary. Cardiologists are blinded, either by economic and/or political considerations. That lack of adequate nutrition is the leading risk factor in heart disease is easily proven, shown by countless studies, but is completely ignored by orthodox cardiology. Damaged arteries must heal. When the surgeon cuts (by-pass operation) or damages the arteries (angioplasty) how can they be surprised that the scab (atherosclerotic plaque) reforms. Any therapy that unnaturally interferes with this healing process (radiation) poses such a great risk to the overall health of the patient that there can be no ethical basis for it whatsoever. Cardiologists believe that their profession is based on strict science and they are taught that there is no value in nutritional therapies.

If nutrition is wrong, no harm is done, if conventional cardiology treatment is wrong, millions have died needlessly. Simply removing plaque (angioplasty) without restoring the vessel to health is like tearing a scab off a wound. Intra-arterial radiation only compounds this basic theoretical problem. One should not remove the scab until after the tissue underneath has started healing. With exposure to radiation, it can’t. The American Heart Association estimates that the cost of heart disease was 326 billion dollars in the year 2000. This includes time lost at work, etc. If medicine had acted on the nutritional results back in 1994 or 1995, more than a million lives and trillions of dollars would have been saved. This makes ignoring nutrition the most costly suppression ever perpetrated by the medico-pharmaceutical complex on humankind. Now that knowledge of the nutritional cure is rapidly spreading, thanks to the Internet, nuclear cardiologists may have found a clever way to preserve the cash cow: intra-arterial high dose radiation. Then they can keep patients perpetually ill. Only in this way can cardiologists guarantee a lucrative income stream that is in great danger of drying up–soon. If your doctor prescribes a therapy such as intra-arterial radiation that interferes with your ability to heal, then the nutritional approach, or any other complementary therapy that works by healing, will not work for you, and may never work. A doctor who advises it should be considered extremely ignorant, incompetent, or worse.