The American Heart Association reported that 1 in 5 deaths in the United States -- a staggering 494,382 deaths -- in 2002 were from coronary heart disease. 1,200,000 new and recurrent cases are recorded each year. Statistics show that approximately 41% of those who experience a coronary attack in any given year will die from it. (National Heart, Lung, and Blood Institute's Atherosciarotic Risk in Communities CARIC study 1987-2000). There are also an estimated 13,000,000 surviving victims of heart attack and other forms of coronary heart disease currently living in the United States.
What Is A Heart Attack?
In their best selling book "Protein Power", Dr. Michael R. Eades, M.D. and Mary Dan Eades, M.D. tell us that a heart attack occurs when, for whatever reason, the blood flow to an area of the heart is cut off or severely diminished.
The heart is a large muscle that contracts rhythmically, pumping blood throughout the body. To understand how hard the heart muscle must work, the authors put forth the following example:
Imagine that you are holding a five (5) pound weight in your hand and that you begin to flex your arm at the elbow, bringing the weight to your shoulder. Your biceps, the muscle on the front of your upper arm, is doing most of the work during this exercise. The various arteries servicing your biceps carry oxygen and nutrient-enriched blood to the working muscle as the veins bear away the waste products and deoxygenated blood.
If you flex your arm repetitively faster and faster, you will ultimately reach the point at which the oxygen needs of the hardworking biceps exceed the capacity of the arteries to supply it. When your muscle begins to get inadequate amounts of oxygenated blood, it begins to hurt, more than likely prompting you to discontinue the exercise and allow your muscle to recover.
Now, if your arm were hooked up to some kind of device that beeped electrical impulses into your biceps to make it contract involuntarily regardless of the pain involved, you can imagine the consequences. The pain would rapidly become excruciating. If the stimulation continued, some of the muscle fibers would begin to die, and ultimately the entire muscle would be damaged irreparably and fail. Your arm would dangle uselessly at your side, unable to contract despite the relentless beeping of the electrical stimulator.
Only in a nightmarish horror novel might this torture be inflicted on a human arm; in real life it is inflicted on human hearts daily. The heart has a built-in, mindless stimulator, the "sinoatrial node", that beeps out an electric current across the body of the cardiac muscle about 72 times per minute. Try contracting your biceps a little faster than once per second and you will realize what an amazing muscle the heart is. It contracts at this rate -- or much faster if, for example, the body needs more oxygen due to exercise or fever -- day in and day out, awake or asleep, never resting until the day you die.
Due to the enormous demands for energy required to continuously contract 72 times per minute throughout life, nature has endowed the heart with an extensive circulatory system: the coronary arteries that wrap around the heart carrying large quantities of oxygen-rich blood to all segments of the muscle. If one of these coronary arteries -- as a result of blood clot, spasm, or plaque growth, for instance -- fails to supply a portion of the heart with enough blood to meet it demands, the heart is in trouble. But the sinoatrial node continues to stimulate the heart muscle, including the segment that is now receiving inadequate oxygenated blood. And as with our biceps, the heart muscle that can't quit beating to rest becomes racked with agonizing pain -- the pain of a heart attack. If the blockage is severe enough and continues long enough, the segment of heart served by the involved coronary artery becomes irreversibly damaged and dies.
Along with the severe pain, the aftermath of coronary arterial blockage typically includes shortness of breath, weakness, nausea, drenching sweat, and the feeling of impending death. Medical science has defined and attached names to all the different degrees and manifestations of this phenomenon: angina pectoris, the pain associated with the lack of heart muscle oxygenation; myocardial ischemia, the situation in which the heart muscle receives inadequate oxygen, but before it is permanently damaged; and myocardial infarction, death of a segment of heart muscle. We lump all these together under the title of heart disease (Protein Power pg. 319-321).
Arteriosclerosis (Hardening Of the Arteries)
Arteriosclerosis is a general term for a condition characterized by thickening, hardening, and loss of elasticity of the walls of the blood vessels. These changes are frequently accompanied by accumulation inside the vessel walls of lipids, e.g., cholesterol; this condition is frequently referred to as atherosclerosis.
Initially lesions are formed on the arterial walls, which results in blistering and the accumulation of low-density cholesterol. This produces higher blood pressure, which facilitates the embedding of cholesterol and calcium in the vessel walls. The fatty material accumulates calcium and produces hard plaques, thus hardening the walls of the vessels. As the vessel walls thicken, the passageways through the vessels narrow, decreasing the blood supply to the affected region.
Constriction of the coronary arteries may affect the heart (see coronary artery disease, heart disease). If the leg vessels are affected, there may be pain with walking and an onset of gangrene. When there is total clotting of a vessel (thrombosis) the result may be a heart attack (if it occurs in the coronary arteries) or stroke (if in cerebral arteries).
Arteriosclerosis risk factors include hypertension, elevated levels of fats in the blood, cigarette smoking, diabetes mellitus, and obesity.
Genetic risks are related to the ability of the body to process (uptake and metabolize) low-density lipids that contain cholesterol. Reduction of body cholesterol to normal levels through cholesterol-lowering drugs and a restricted-fat diet is usually prescribed. The latter generally entails substitution of vegetable fats for animal fats, but an exception may be "trans fat", artificially hydrogenated vegetable oils found in margarine and vegetable shortening, which studies have linked to increased risk of coronary disease.
Treatment of hypertension, stress management, and cessation of smoking are also important. Increasing consumption of antioxidants and folic acid may be protective. Surgical treatment that bypasses clogged areas or procedures such as angioplasty are sometimes necessary; gene therapy that forces the growth of new blood vessels bypassing an area has also been used. Exercise often can increase utilization of excess low-density lipids. Although the relationship between blood cholesterol levels and arteriosclerosis is not fully understood, the utilization of low-density lipids appears to be a primary indicator of the risk of arteriosclerosis.
Angioplasty
Angioplasty refers to the re-opening or unclogging of a blood vessel that is significantly narrowed by plaque. It is most often used in patients with obstruction(s) in one or two coronary arteries. This is called called "single-vessel" or "double-vessel disease," respectively. Coronary artery bypass surgery remains the treatment of choice for severe multi-vessel disease, where three or more coronary arteries are significantly obstructed.
Angioplasty in most cases involves a procedure where a thin catheter attached to a tiny balloon is inserted into the artery that is blocked. When the catheter reaches the site of blockage, the balloon is inflated, flattening the plaque against the arterial wall and enlarging or re-opening the vessel. This technique is called ercutaneous transluminal coronary angioplasty (PTCA) or balloon angioplasty.
At times procedures may be used in conjunction with PTCA that use small surgical instruments to strip the inner lining of a blood vessel to remove plaque from the vessel. Another procedure uses the forceful injection of fibrinolytics that inject drugs to break down fibrin in blood clots.
In people with a recent heart attack, an alternative to thrombolytic therapy is immediate coronary angiography followed by percutaneous angioplasty of the lesion responsible for the heart attack. This treatment is called "primary PTCA." Primary PTCA is considered most strongly in individuals who have evidence of an acute Q-wave heart attack, those who can undergo PTCA within 12 hours of the first symptoms (or beyond 12 hours if pain persists) or can have the procedure performed by a skilled and experienced operator in a setting where emergency surgery can be performed.
Other individuals who may benefit from primary PTCA include those in whom thrombolytic therapy is not appropriate due to risks.
Coronary angiography and evaluation for possible PTCA is also useful at a later point for some individuals. These especially include those who are experiencing angina after the heart attack or instability of cardiovascular parameters (e.g., unstable blood pressure), or scheduled for certain mechanical repair from a heart attack.
Coronary angiography and PTCA are not considered useful within days of having received thrombolytic therapy in survivors of a heart attack who are not thought to be appropriate candidates for coronary revascularization(the reestablishment of blood supply to a portion of heart muscle).
Stent
A stent is a small, coiled wire-mesh tube that can be inserted into a blood vessel and expanded using a small balloon during a procedure called angioplasty (PTCA). A stent is used to open a narrowed or clotted blood vessel, most often an artery in the heart.
When the balloon inside the stent is inflated, the stent expands and presses against the artery walls. This traps any fat and calcium buildup against the walls of the artery, allows blood to flow through the artery, and helps prevent the artery from closing again (restenosis). It can also help prevent small pieces of plaque from breaking off and causing a heart attack. A stent can help prevent the lining of the artery from tearing or rupturing, which can lead to a stroke.
To insert the stent, a flexible, thin tube (catheter) is passed through an artery in the groin or arm into the narrowed artery. A small balloon positioned inside the stent is inflated. The pressure from the inflated balloon opens the stent and pushes it in place against the artery wall. Newer stents are coated with a medication to more effectively prevent restenosis.
Coronary Artery Bypass Surgery
Coronary artery bypass surgery, also known also as "bypass surgery" and coronary artery bypass grafting (CABG), is an operation in which a blood vessel is taken from elsewhere in the body (usually a vein from the leg or an artery from the chest) the blood vessel is then used to create an alternate pathway of blood or bypass to the heart.
The procedure is extensive surgery that often requires opening the chest and temporarily stopping the heart. During this time, blood flow is maintained to body tissues by a heart-lung machine, which replicates the pumping action of the heart. (A newer procedure allows the heart to continue to beat, but this procedure is not as widely used.)
One end of the transplanted vessel(called a graft) is connected below the blockage in the coronary artery while the other end is attached to the aorta, the major artery that carries blood away from the heart and into the body. The bypass procedure is repeated for each blocked coronary artery. For example, "triple bypass" means that three grafts have been placed).
Bypass surgery is generally reserved for individuals whose coronary artery disease cannot be adequately treated by cardiac medications or cannot be treated with angioplasty. Also, it may be used for individuals who suffer from intractable or unstable angina. These individuals usually have significant obstruction of the three main coronary arteries depressed pumping action or blockage of the left anterior descending artery. They also have typically not responded to intensive medical treatment for angina or have just suffered an acute heart attack.
Bypass surgery is performed in people with an evolving heart attack when pain and ECG findings are unstable and the individuals have had failed angioplasty (They still have persisting pain or continue to be unstable after angioplasty). It is also performed in people who are undergoing repair of mechanical complications such as a tear in the wall dividing the ventricles (ventricular septal defect) or heart valve insufficiency ("leaky" heart valves) Other individuals who may benefit from CABG after a heart attack are those who are suffering from cardiogenic shock or who remain unstable after PTCA.
While bypass surgery can limit damage in people with an acute heart attack, it does not cure the underlying coronary artery disease. Many still require medications after CABG. Lifestyle modification and cardiac rehabilitation are recommended. Recovery time following CABG is influenced by a person's age, overall health, and cardiac function.
Studies have shown that after angioplasty, the coronary artery that was dilated will usually become narrowed again and may close off. The frequency with which this happens is about 50%. How often this will result in repeat symptoms is not precisely known. Several reports describe recurrences of cardiovascular events including death, heart attack, unstable angina, repeat angioplasty and coronary artery bypass surgery.
Aside from the acute and subacute complications of angioplasty and bypass surgery, a major concern is the acceleration of the arteriosclerotic process (see arteriosclerosis) in the coronary arteries that are treated.
For example, vessels that are bypassed often show rapid progression of the blockage process which originally led to the patient's symptoms. More importantly, collateral vessels that had developed over a period of time to compensate for a narrowed artery will usually disappear following bypass surgery. Thus, the lack of blood supply to the heart muscle may actually be worse off following such surgery.
The importance of these collateral vessels is illustrated by the fact that when a coronary artery is severely narrowed, and then becomes completely blocked, it has little effect on cardiac function. This is because there are enough collateral vessels to make up for the deficit in blood flow. In contrast, when a coronary artery is only mildly narrowed, and closes off suddenly, it is likely the patient will have a myocardial infarction or even die: because the mildly narrowed coronary artery has not yet had a chance to develop new collateral vessels.
Medications Used to Treat Heart Disease
Medications used to treat heart attacks in the hospital are also used to relieve symptoms after hospital discharge. Medications are used to relieve chest pain and anxiety, limit the size of the heart attack, reduce the work of the heart and to prevent and treat complications.
Medications To Relieve Chest Pain And Anxiety
Major medications used to relieve chest pain include nitrates such as nitroglycerin and narcotic pain relievers such as morphine. Benzodiazepines, which are minor tranquilizers or antianxiety agents can help relieve anxiety.
Nitrates, such as nitroglycerin, are used to treat chest pain associated with a heart attack as well as angina. Nitrates work by relaxing smooth muscle, including the smooth muscle in the walls of blood vessels. This causes them to dilate or open up, which improves blood flow to the heart and rest of the body. This widening of arteries also lowers resistance to blood flow and blood pressure, which lowers the work of the heart. Dilation of veins decreases the amount of blood flow returning to the heart, which also decreases the heart's work load. Nitrates also improve blood flow to the heart and decrease work of the heart. Both of these events relieve pain due to inadequate blood flow (and thus, oxygen supply) to heart muscle.
Nitrate medications comes in a variety of forms which include pills that dissolve under the tongue, pills that are swallowed, mouth sprays, ointments or creams, and skin patches.
Intravenous nitroglycerin is recommended for the first 24 to 48 hours after a heart attack, in patients with an acute heart attack complicated by congestive heart failure or those with a large heart attack affecting the front wall of the heart(called an anterior-wall myocardial infarction). This is also recommended for those who may have persisting insufficient blood flow to heart muscle, as detected by pain and ECG or hypertension or high blood pressure.
Use of nitroglycerin beyond 48 hours is useful if the chest pain returns or if persistent lung congestion due to heart failure occurs. Individuals with an abnormally low blood pressure or slow heart rate should not receive nitrates because of the nitrates' tendency to lower blood pressure. Side effects of nitrates include headache and occasional faintness.
Morphine and other narcotic pain relievers are used to relieve chest discomfort associated with a heart attack. Repeat dosages of morphine can be given intravenously frequently if breathing remains normal and no signs of toxicity occur. Side effects of narcotic pain relievers include nausea and pruritus (itching).
Medications To Limit The Size Of The Heart Attack: "Clot Busters"
During a heart attack, most damage to heart muscle occurs within the first six hours. Treating a heart attack during the first two hours is essential for preventing or reducing heart muscle damage.
Most heart attacks are caused by a blood clot blocking a coronary artery. Using thrombolytic agents or "clot busters" that can break down blood clots and restore blood flow through the artery can limit heart muscle damage.
Thrombolytic agents include streptokinase, anisoylated plasminogen-streptokinase activator complex (antistreplase), tissue plasminogen activator (t-PA). Although all these medications work in slightly different ways, they all activate an enzyme called "plasmin," which breaks down fibrin in blood clots. Giving a clot buster within several hours of an acute heart attack restores blood flow and significantly reduces damage in most cases where a coronary artery has been blocked by a blood clot. The earlier these drugs are used, the greater the benefit.
Giving thrombolytics within one hour after a Q-wave heart attack restores blood flow in up to 80 percent of cases. Using thrombolytics within two hours of the onset of chest pain cuts the death rate to half that of patients who received therapy after six hours of pain. Minutes count!
The goal of many medical facilities is to have a "door-to-needle" time of 30 minutes of less -- from when a patient enters to when he or she receives the clot buster medication.
Clot buster therapy is sometimes followed by treatment with blood thinners such as heparin to prevent future clot formation. Blood thinners can be given intravenously or under the skin, depending on type of drug and the patient's risk for future problems due to blood clots.
Thrombolytic treatment is appropriate for patients with an acute heart attack who can begin treatment within 12 to 24 hours of the onset of symptoms (preferably less than 12 hours), those who have ST segment elevation in two or more leads on an electrocardiogram(ECG) -- consistent with an acute Q-wave heart attack affecting the entire thickness of heart muscle -- and those who have other ECG changes consistent with a heart attack affecting the front wall of the heart.
Thrombolytics probably do not help people with pain that has lasted for longer than 24 hours or those who only have ST segment depression on ECG.This ECG finding is suggestive of a non-Q-wave heart attack, which often only affects the innermost layer of the heart muscle.
People at risk for bleeding should not receive thrombolytic agents. These include people who are recovering from recent surgery, have active bleeding from stomach ulcers, very high blood pressure, a history of a recent stroke, head injury, or a bleeding disorder.
An alternative to thrombolytic therapy is coronary angiography followed by percutaneous transluminal coronary angioplasty (PTCA), referred to as primary PTCA. Also, other drugs can help limit the size of the damage by reducing the work load of the heart.
Medications To Reduce The Workload Of The Heart
How well the heart works after a heart attack depends largely on how much heart muscle was damaged. Medications that decrease the workload and the oxygen needs of the heart can reduce the size of the area of dead heart muscle and optimize the amount of remaining healthy heart muscle. Drugs that decrease the workload of the heart include nitrates, beta blockers,and angiotensin converting enzyme (ACE) inhibitors.
Beta blockers have long been used in the treatment of angina and hypertension (high blood pressure). Intravenous beta blockers given within the first several hours of the onset of a heart attack improve the prognosis (outcome) by: reducing the size of the infarct (area of dead muscle cells), lowering the chances of a repeat heart attack, and/or reducing the risk of deadly abnormal heart rhythms such as ventricular fibrillation. All of these benefits reduce the risk of death.
Treatment with beta blockers within the first 24 hours of the onset of a heart attack is recommended for all patients who can tolerate them. Beta blocker therapy is especially useful in individuals with continuing or recurrent pain or abnormally fast heart rhythms called tachycardias.
Beta blockers reduce the heart's workload by slowing the heart rate and reducing how hard the heart pumps (called contractility). All of these effects lower blood pressure as well as heart muscle oxygen requirements.
Due to the actions of beta blockers on the heart, blood vessels, and lungs, some people may not be able to tolerate beta-blocker therapy. This may include those with abnormally low blood pressure (hypotension), abnormally slow heart rate (bradycardia), heart failure, asthma or chronic obstructive pulmonary disease (COPD). Side effects of beta blockers may include: fatigue, depression, erectile dysfunction, hyperglycemia or high blood sugar level.
Other side effects may include an undesirable change in blood lipid levels, such as increased triglyceride levels and lower levels of "good" (HDL) cholesterol. Some of these side effects can be reduced by lowering the dosage, and/or with the use of angiotensin converting enzyme (ACE) inhibitors.
Angiotensin converting enzyme (ACE) inhibitors are drugs used in the treatment of hypertension (or high blood pressure), heart failure, diabetic nephropathy (kidney disease due to diabetes) and myocardial infarction or heart attack.
Using angiotensin converting enzyme (ACE) inhibitors after a heart attack limits undesirable structural changes to the heart chamber that pumps blood through the body (called "ventricular remodeling"). It also lowers the frequency of complications such as recurrent angina and heart failure, and reduces the risk of death from the heart attack. And it reduces the risk of a subsequent heart attack.
The benefits of ACE inhibitor therapy add to the benefits of treatment with beta blockers (see above) and aspirin, and are greatest in individuals with impaired ventricular function (inadequate heart pumping), and full-blown heart failure.
ACE inhibitors should be given 24 hours or more after stabilization with thrombolytic drugs, and continued indefinitely in individuals with impaired ventricular function. The ACE inhibitors work by blocking the conversion of the inactive angiotensin I to active angiotensin II.
The resulting lower level of angiotensin II circulating in the bloodstream reduces blood pressure, and the work of the heart, because of less blood vessel constriction or narrowing caused by angiotensin II. This reduces resistance to blood flow through blood vessels, putting less strain on the heart. Less retention of sodium and water by the kidneys in response to angiotensin II results in a lower volume of blood that has to be pumped by the heart.
The most common side effect of ACE inhibitors is a reversible dry cough. Other side effects may include headache, dizziness, fatigue, hyperkalemia or high potassium levels. Infrequent and rare side effects include a reduction in the number of white blood cells (neutropenia), and a reversible skin rash with one type of ACE inhibitor.
Medications To Prevent And Treat Complications
These drugs embody an assortment of agents used to treat complications of a heart attack. They include aspirin, antiarrhythmic agents, drugs for heart failure, and anticoagulants (blood thinners).
Aspirin decreases clot formation by reducing platelet adhesion. This is the "sticking together" of a type of blood cell involved in blood clot formation.
Aspirin therapy has been shown to decrease the risk of death associated with a heart attack as well as reduce the risk of a subsequent heart attack. Unless contraindicated, aspirin should be started immediately and continued indefinitely on a daily basis. Other drugs that reduce platelet adhesion may be substituted if the person is allergic to aspirin or does not respond to treatment.
Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) are useful for treating chest pain due to pericarditis (inflammation of the sac that encloses the heart), which may occur after a heart attack.
Antiarrhythmic agents refers to a variety of drugs used to treat abnormal heart rhythms (arrhythmias) associated with a heart attack. These drugs are divided into four classes:
Class I: These are sodium channel blockers including drugs such as quinidine, procainamide, and lidocaine. These agents must be used with caution as they can also depress left ventricular function (heart pumping) and promote or cause arrhythmias.
Class II: These drugs are beta-blockers, and examples include atenolol and metoprolol. These agents are used to control supraventricular tachycardias (arrhythmias originating above the ventricles), and also help to suppress dangerous ventricular arrhythmias such as ventricular tachycardia and ventricular fibrillation.
Class III: Examples of these drugs are amiodarone and sotalol. Amiodarone is the most powerful antiarrhythmic drug, but its side effects limit its use. Sotalol is also a beta-blocker, with side effects and other actions similar to those of other beta-blockers. It is used to treat atrial fibrillation and atrial flutter as well as ventricular arrhythmias.
Class IV: These drugs are calcium channel blockers, which slow the heart rate and dilate or open up blood vessels. These drugs are used to control abnormally rapid rhythms such as atrial fibrillation, as long as signs of heart failure or heart blockage are not present. Examples include verapamil and diltiazem.
In addition to the above four classes of antiarrhythmic drugs, there are also some miscellaneous drugs used (such as Digoxin, which increases the strength of heart muscle contractions and is useful in the treatment of heart failure). Because digoxin also slows conduction of the heart's electrical impulses, it is also useful in controlling atrial fibrillation, atrial flutter, and atrial tachycardia. Another drug, Adenosine, slows or blocks the conduction of electrical impulses. Since it is only available in intravenous form and only works for a short time, adenosine is only used as acute treatment for supraventricular tachycardias.
Most of the above drugs treat rapid or irregular heart rhythms. Slow heart rhythms (bradycardia) or asystole (cardiac standstill) are treated with atropine or similar drugs. In some cases, a pacemaker may be necessary.
Attending physicians should know that selection of the antiarrhythmic drug depends on the type of abnormal rhythm and on clinical circumstances. Another way of treating arrhythmias is electrical cardioversion. This involves application of electrical shocks to the chest to convert the abnormal heart rhythm to a normal rhythm. Electrical cardioversion is used to stop all life-threatening tachycardias or rapid heart rhythms. Cardioversion of ventricular fibrillation to sinus rhythm is referred to as defibrillation. Cardioversion is also used to stop atrial flutter or atrial fibrillation associated with cardiovascular instability or ischemia.
Drugs commonly used to treat heart failure that may occur with a heart attack are diuretics, which reduce the blood volume by causing the kidneys to get rid of more sodium and water.
Individuals with very low blood pressure due to cardiogenic shock may require treatment with inotropic agents, which are drugs that increase the force of heart contraction. Two examples are dopamine and dobutamine.
These drugs increase the vigor of heart pumping, which in turn increases the amount of blood pumped. The higher cardiac output increases blood pressure and allows more body tissues to receive adequate blood flow.
Anticoagulants (blood thinners) differ from thrombolytic agents in that they prevent blood clots from forming, as opposed to dissolving existing clots. Good candidates for treatment with anticoagulants such as heparin after a heart attack include those who are undergoing percutaneous or surgical revascularization -- the reestablishment of the blood supply to a portion of muscle, those who are receiving the thrombolytic agent alteplase or receiving nonselective thrombolytic agents (such as streptokinase, urokinase, or antisteplase) but considered at high risk for complications due to blood clots traveling through the bloodstream.
People receiving nonselective thrombolytic agents who are not at high risk for such blood clots may still benefit from subcutaneous heparin, which is heparin administered under the skin instead of in the veins. The routine administration of intravenous heparin does not appear to benefit these individuals.
Why Lesions Form On Arterial Walls Causing Arteriosclerosis and Heart Disease
There are thousands of species of animals on Earth and only four do not produce their own ascorbates. Many scientific studies have shown that many of the body's systems require ascorbates to function properly. Those systems, in the absence of ascorbates, will fall into dysfunction and disrepair. Ascorbate deficiency has been irrefutably linked to the world's #1 killer heart disease.
Ascorbate deficiency causes microscopic cracks, or lesions, to develop in arteries. Another term for the condition is "sub-clinical scurvy." The body's response to these lesions is to "patch" them with the lipoprotein we know as LDL (lower-density lipoprotein) cholesterol. If the body did not patch these lesions, we would die from internal bleeding.
(Note: LDL cholesterol has been maligned as the "bad cholesterol" because cardiologists find it lining and, eventually, blocking blood vessels and arteries. The body creates "good" HDL (high-density lipoprotein) cholesterol to carry fats straight to the liver where they are eliminated as bile acids through the gall bladder and, ultimately, the intestines).
As time elapses, the cracks become more numerous and the older LDL cholesterol patches harden into plaque. This process causes the diameter of the arteries to become narrower.
This is why "high blood pressure" is usually the first sign of heart disease -- it's a law of nature that when the flow of liquid is restricted, increased pressure results.
Eventually, the restriction can become a blockage, shutting off the flow of blood to tissue in certain areas of the body. This eventuality damages tissue and leads to angina, strokes or heart attacks. Plaque and clumping blood can also break away from their moorings, travel to the heart and cause a heart attack.
The work of Nobel Prize laureate Dr. Linus Pauling has documented that one of the basic causes of heart disease is ascorbate deficiency, which causes lesions in blood veins, vessels, and arteries, and that the body's response is to patch the lesions with LDL cholesterol to prevent us from bleeding to death. This process causes restrictions in blood flow which causes high blood pressure: eventually resulting in angina and heart attack.
For the last four decades of his illustrious career, Dr. Pauling was concerned with the question of how much Vitamin C is required in humans to optimize health. He reasoned that since humans are one of only four species that have lost the ability to make Vitamin C, we should obtain from our diets at least as much as other species make on their own. He concluded that the Recommended Daily Allowance (60 milligrams) is pitifully inadequate. Dr. Pauling believed that humans need 6 to 20 grams of Vitamin C daily, depending on body size. He calculated his own daily dose at 20,000 milligrams (20 grams) which he took religiously until his death at age 93.
Insulin: the Forgotten Factor In Arteriosclerosis and Heart Disease
Insulin is a hormone that is produced and released into the blood by the pancreas. It affects virtually every cell in the body. There are whole chapters in every medical biochemistry and physiology textbook devoted to insulin. Whole textbooks are written about its myriad activities. Insulin regulates blood sugar, true, but it also does much much more. It controls the storage of fat, it directs the flow of amino acids, fatty acids, and carbohydrate to the tissues, it regulates the liver's synthesis of cholesterol, it is involved in appetite control, it drives the kidneys to retain fluid, and it even functions as a growth hormone. It is the master hormone of metabolism and is a substance absolutely essential to life; without it, you would quickly die.
On the other hand, insulin has a dark side. In the proper amount it is life sustaining; too much of it creates enormous health problems. Reams of scientific studies now implicate insulin as a primary cause or significant risk factor in the development of coronary heart disease.
Insulin exerts its influence in several ways in the development of plaque in coronary arteries, starting with elevated levels of LDL cholesterol in the blood. Although arterial damage and heart disease can occur in the face of normal -- or even low -- blood cholesterol, elevated LDL levels usually hasten their onset. And insulin, by its action on the cholesterol synthesis pathway located within the cells, helps to create and sustain excess amounts of LDL in the blood.
Insulin acting as a growth hormone also encourages the growth of smooth muscle cells in the coronary arteries and their migration into the area of plaque formation. This not only accelerates the development of plaque but increases the thickness and rigidity of the arteries as well. Once these smooth muscle cells travel into the developing fatty streak, and plaque growth continues, insulin stimulates the increased synthesis of collagen and other connective tissues that make up the large part of the forming mass of plaque. At the same time insulin enhances the cholesterol synthesis within the plaque lesion: the source of its greasy appearance.
Insulin and Plaque Formation
A research team in the early 1960s, led by Dr. Anatolio Cruz in what is now a classic experiment, demonstrated the changes wrought by chronically elevated levels of insulin. His team of scientists injected insulin into the large arteries of the legs of dogs: each day each dog was injected with insulin the artery of one leg and the same-size dose of sterile saline in the other. This was done daily for almost eight months.
When examined the arteries injected with the insulin were found to have a pronounced accumulation of cholesterol and fatty acids along with a thickening of the inner arterial lining while the opposite arteries, injected with saline, remained normal. These profound changes were induced with a relatively small dose of insulin given only once a day for a little over seven months. Can you imagine the changes that might have been found if the experiment had been able to keep the insulin level consistently elevated for several years! It should not be difficult to picture the changes in our own coronary arteries after many years of chronic hyperinsulinemia... which affects over 14,000,000 Americans.
Continuous elevated blood levels of insulin due to "insulin resistance" has created an enormous health crisis for Americans and Western society. Coupled with damaged coronary arteries from sub-clinical scurvy, the insulin factor exacerbates the risk of heart disease. Elevated blood levels of insulin can be lowered by reducing the intake of carbohydrates in our diets. However, the proper amounts of Vitamin C needed to stop and repair damage to coronary arteries must be done through supplementation.
Advanced Scientific Health (ASH), a cooperative research organization, provides its members an ascrobate formula to combat heart disease and arteriosclerosis brought on by sub-clinical scurvy or ascorbate deficiency.
Your body must have vitamin C (ascorbic acid) to build strong collagen, the main structural protein in the body that makes the framework for bone, muscle fiber, tendon, ligament, skin, hair, and scar tissue to heal wounds. Without adequate vitamin C the collagen that is made is weak and of poor structural quality. It tears easily. When people become deficient in vitamin C, they bruise easily, their teeth loosen and fall out, they lose their hair, their gums bleed, their wounds don't heal well, their joints weaken, and finally they usually hemorrhage (from weak blood vessel walls) and die.
The disease this vitamin deficiency causes is called scurvy, and it nearly destroyed the navies of many countries until the British recognized that they could prevent it by making sure their sailors ate plenty of limes and lemons while at sea.
This preventive measure created a popular misconception that citrus fruits are the only good dietary source of vitamin C. However, Arctic explorer Vilhjalmur Stefansson conclusively proved that wrong in the late 1920s. Fresh, lightly cooked meat and fish, he found, contain enough of a vitamin C-like substance (mineral ascorbates as well as all other critical micronutrients) to prevent scurvy and other deficiency diseases. The Journal of the American Medical Association documented that Stefansson, who spent one full year on a drastic diet of nothing but fresh meat and water, not only did not die as predicted but emerged fitter, leaner, with lower cholesterol counts (about the only laboratory marker for heart disease available in the late 1920s), and healthier in every regard.
Eskimos eat very little carbohydrates or citrus fruit -- in fact none at all during the winter -- and survive nicely to a ripe old age. Although their traditional diet is composed of a large quantity of protein and an enormous amount of fat, Eskimos suffer from no scurvy, and very little heart disease, diabetes, obesity (despite the cartoons), high blood pressure, and all the other diseases we associate with a more civilized lifestyle. Furthermore, Eskimos don't have metabolic systems from an alien planet; they have the exact same biochemistry and physiology that we do.
Ascorbates come in many forms, the cheapest being ascorbic acid. However, even moderate quantities of ascorbic acid taken orally can produce a variety of discomforts. The ASH formula "NO FOOL I" is composed of four mineral ascorbates and can be tolerated in much higher dosages. Sodium Ascorbate and Potassium Ascorbate are used because extra cellular fluids are rich in both sodium and potassium. Two other ascorbates -- Calcium and Magnesium -- are also in the formula. One teaspoon contains 1.6 grams (1,600 milligrams) of these ascorbates.
NO FOOL I is the basis for a number of different functions in the body, but for this discussion it is taken daily: to heal the arterial cracks we discussed previously and to prevent their recurrence. Dr. Linus Pauling and Dr. Matthias Rath found that three grams were sufficient to prevent the world's number one killer: heart disease. People already suffering have reported doubling and sometimes tripling that amount for a while as the arteries and plaque correct themselves.
Dr. Pauling and Dr. Rath called the substances that treat chronic scurvy and destroy existing plaques Lp(a), binding inhibitors. Also Vitamin C, to increase collagen production and to improve the health and strength of arteries. Their treatment for cleaning existing atherosclerotic plaques is a large dosage of another essential nutrient, the amino acid L-lysine. Dr. Pauling recommended that heart patients take between 2,000 and 6,000 mg of L-lysine daily with their vitamin C (more if serum Lp(a) is elevated). Neither vitamin C nor L-lysine have any known lethal dose. These substances taken together are clinically effective.
Dr. Pauling recounts the first cases where his high Vitamin C and L-lysine therapy quickly resolved advanced cardiovascular disease in humans. The effect is so pronounced, and the inhibitors are so nontoxic, that he doubted a clinical study was even necessary. Recently, the amino acid L-proline was found to be an even more effective Lp(a) binding inhibitor than lysine.
Each teaspoon of NO FOOL I contains 1,500 milligrams of L-Lysine and 250 milligrams of L-Proline.
Don't Make Your Vitamin C Compete With Sugar
Many people, especially diabetics, are not absorbing vitamin C and probably other nutrients from their blood. Why? Because vitamin C is structurally similar to glucose and the vitamin has a short half-life in the bloodstream. It should concern medical professionals that vitamin C and glucose molecules share the same insulin-mediated tunneling mechanism into cells through the membrane. Therefore, since all nutrients enter the cells through the cell membrane it is likely that they must compete with glucose (sugar) to enter the cell.
In the 1970s, Emeritus Professor John T. A. Ely, University of Washington, proposed his Glucose-Ascorbate Antagonism (GAA) theory that predicts high glucose levels hinder vitamin C entry into cells. Animals which make their own vitamin C use dietary glucose as the raw material and the ascorbate and glucose molecules are similar. The similarity extends past molecular structure to the way they are attracted to, and enter, cells. Both molecules require help from the pancreatic hormone insulin before they can penetrate cell membranes using special "pumps." The name for the process that propels glucose and Vitamin C (the reduced form) through cell membranes is Insulin-mediated uptake.
Professor Ely studied the insulin-mediated uptake of glucose and vitamin C using white blood cells. White blood cells have more insulin pumps and they may contain 20 times the amount of vitamin C as ordinary cells. Dr. Ely explains that both glucose and vitamin C molecules compete, but all things are not equal. The evolutionary "fight-or-flight" response favors glucose entry into cells at the expense of vitamin C. Because of this antagonism between sugar and Vitamin C, Ely recommends a low-carbohydrate, low-processed sugar diet.
Professor Ely advised Linus Pauling of the GAA theory and its prediction that Vitamin C would be less effective fighting colds in those who did not restrict their sugar intake. Recently, he and his associates conducted a study on the common cold to test the GAA theory. Sugar and refined carbohydrates were restricted in the subjects. According to Dr. Ely, the remarkable results showed an overwhelming preventive and curative property of vitamin C against the common cold in subjects with reduced sugar intake.
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