A half a million Americans undergo coronary bypass surgery each year.
There are also many others who are treated with surgery as a 'preventive strategy' to remove the arterial plaque that causes blockage in coronary arteries. And of course there are those who remain undiagnosed but who will ultimately suffer a heart attack.
All told, surgery is an expensive method to treat cardiovascular disease.
The Affordable Care Act is centered on how often and how much to pay for treatments. That doesn't sound like they are dealing with the real problem.
The best way to improve heart health is to maintain fitness in life. While this may be difficult, considering the demands of living in today's world, there really is no other choice.
Without improvement in individual health, this nation is borrowing away its future.
Mandate exercise as a precondition for medical benefits.
Unhealthy people who choose to stay unhealthy will have to pay for their own treatment or it will be denied.
The only reason a person should be denied medical coverage is when they refuse to alter the behavior that caused the illness.
Universal coverage means the government can force its citizens to be healthy.
America needs to get healthy.
With future savings from illness, America can turn its attention to the environment or its crumbling infrastructure.
Health needs to be given more value. Illness is what pays now! All levels of it. From the causative agents to the drugs used for treatment.
The best practices to prevent heart disease are a lower weight, a colorful diet and a pattern of daily, regular exercise.
Intense, daily exercise ensures a healthy heart.
It must be pointed out that the absence of symptoms does not mean the absence of arterial plaque. It is a silent killer.
The buildup of fatty deposits within walls of blood vessels occurs without any symptoms.
Preventive treatment is the use of pharmaceutical drugs and invasive surgeries to unclog, blocked and narrowed arteries.
A recent report has sent shock waves through the hospital and medical community.
The study indicated that this dual approach of surgery and drugs was no more effective in reducing the risk of heart attacks than drugs alone.
The correct approach is to improve the diet, remove the stress and get moving.
The high incidence of heart disease among Americans is more the result of inactivity than actual weight.
As a consequence of this reality, the loss of weight by those at risk for cardiovascular disease may not provide as much of a preventive effect as previously thought.
In other words weight loss by itself is not enough to prevent heart disease, it must be coupled to increased exercise.
High cholesterol levels remains the prime culprit and is strongly implicated in causing coronary heart disease.
It has been suggested that only 1% of affected individuals can claim that their hypercholesterolemia is the result of heredity, the other 99% develop this condition because of their choices in lifestyle and dietary habits.
While adult-onset diabetes is the result of an imbalance in carbohydrate metabolism, heart disease is due to an imbalance in fat metabolism. Since they are both nutritonal diseases, they are both preventable.
To best understand the dynamics of heart disease a brief review of its biology is presented below.
The Mechanics of Heart Disease
Arteries over time, undergo a loss of elasticity and a thickening of their lining. A process associated with the natural process of aging. This condition is termed arteriosclerosis. In contrast, atherosclerosis refers to pathological conditions that obstruct the flow of blood in the coronary, carotid and femoral arteries.
Coronary artery disease is the result of such a lesion blocking the flow of blood to the heart to the heart itself. As a 24-7 working mucle, the heart needs nourishment. Any impediment to providing it, causes serious disease.
Atherosclerosis is a nutritional, chronic disease that afflicts over half the US population and is the leading cause of death in the industrialized world. It is particularly lethal in 40-60 year old men.
Women develop the symptoms 10 years later.
Atherosclerosis begins with elevated level of plasma lipids, especially LDL-cholesterol. I use the term 'lousy cholesterol' to differentiate it from HDL-cholesterol or the healthy version.
Atherosclerosis is a three-stage process that begins with an imbalance in lipid chemistry and ends up as an occluded blood vessel. Prevention is based on restoring balance to fat metabolism and protecting the lipoprotein from oxidative attack.
The following summarizes the three stages of atherosclerosis.
1. The disease originates with the accumulation of plaque or fatty deposits within the walls of coronary blood vessels. A fatty streak is the first observable sign. There are no symptoms and can only be seen with the aid of a microscope. The streak is composed of foam cells, which owe their appearance to the large cytoplasmic droplets of cholesterol they contain.
2. Once a fatty streak has developed it becomes the foci for inflammatory attack, resulting in the formation of a fibrous plaque that contains connective tissue, smooth muscle cells and necrotic debris along with the lipids. Once this undergoes calcification, these atherosclerotic lesions will narrow the lumen of the artery, restricting the flow of blood.
3. In the third stage, a thrombus or clot forms that blocks and closes one of the coronary arteries. The heart then becomes susceptible to failure because of an insufficient delivery of blood.
Exercise maintains the health of the heart. Like any other muscle, the more it is used, the stronger it becomes. It is therefore essential that the arteries that feed it, remain free of obstruction.
To improve lipid profile, a dietary strategy that reduces the intake of saturated fat and substitutes monounsaturated olive fat in its place, should be followed. This is best achieved with a colorful, complex, carbohydrate diet, rich in fish oils and high fiber foods. In addition policosanol, a dietary supplement derrived from sugar cane is thought to lower lipoproteins as much as the statins, the pharaceutical drugs of choice in treating hypercholesterolemia.
Along with the reduction of saturated fat and the elimination of trans-fatty acids, this strategy recommends cold-water fish and dietarry supplements that contain the omega-3 fatty acids, eicopentenoic (EPA) and docosahexenoic (DHA) acids. Omega-3 fatty acids reduce the synthesis of unhealthy cholesterol and the inflammatory prostanoids.
Omega-3 fats also represses the synthesis and improves the removal of lipoproteins. Oil of primrose, flaxseed oil, borage oil and some nuts are other good sources of omega 3s. In addition, high fiber foods like edible algae (kanten) are recommended to prevent the absorption of cholesterol from the intestine. These dietary adaptations, combined with regular, intense exercise, represents the best method to prevent an imbalance in fat metabolism and the resulting coronary artery disease.
Healthy heart diets attempt to eliminate all fats in the diet by replacing saturated fat with carbohydrates. While this substitution does reduce the lousy LDL-cholesterol levels, it lowers the healthy HDL faction as well. This dietary practices therefore does not alter the actual LDL/HDL ratio. A favorable ratio of high HDL to low LDL is the factor that actually reduces atherosclerosis. Therefore by substituting monounsaturated fat for saturated fat, LDL can be reduced without affecting HDL levels.
This produces the most desirable lipid profile.
Excess calories, particularly fat calories, stimulates the liver to produce cholesterol. Substituting complex carbohydrates and high fiber foods instead of protein and fat is a good practice. These foods include beans, pasta, rice and whole grain breads. A diet rich in complex carbohydrates and fiber lowers cholesterol levels by preventing its absorption. In fact, certain saponins, a natural substance found in beans and plants (sprouts, soybeans and yam), tend to interfere with cholesterol absorption from the intestine promoting its elimination. This failure to absorb cholesterol and its subsequent excretion from the body indicates that these colorful carbohydrate foods can delay or even prevent heart disease.
One of the goals of preventive nutrition is to prevent the formation of atheromatic plaques, reduce its progression or cause the regression of existing plaques. Dietary strategies to achieve this include high fiber, the reduction of saturated fat, consumption of fish known to contain the omega-3 fatty acids, eicopentenoic (EPA) and docosahexenoic (DHA) acids.
Heart disease is initiated by the formation of plaque in coronary blood vessels.
Once formed, plaque becomes the foci of inflammation and around it, a clot forms.
Plaque results from the deposition of cholesterol in the form of oxidized-LDL on the intima or inner lining of arteries. By preventing the oxidation of LDL in the first place, the formation of plaque and the subsequent inflammatory attack on it, never happens. Now that's prevention!
Antioxidants reduce the risk of heart disease and other chronic diseases by preventing oxidations. That is the main premise of this philosophy.
Vitamins E and C, the mineral selenium and beta-carotene are the antioxidants recommended by medical authorities to help prevent heart disease. This strategy further adds colorful botanical antioxidants (flavonoids, proanthocyanidins) and healthy fats to their list. These botanical buffers, which protects plants from the harmful rays of the sun, can also provide powerful antioxidant protection to humans and provide a preventative effect on atherosclerosis and coronary heart disease.
Most of the research on LDL oxidation and nutrient antioxidants has been done using alpha-tocopherol, the most biologically active and prevalent form of vitamin E. Alpha-tocopherol traps peroxyl free radicals and thus is a chain breaking antioxidant. Alpha-tocopherol is the predominant lipophilic (fat soluble) antioxidant in tissues and is found embedded within the LDL molecule.
Good health requires that the body’s protective energy force stimulate the antioxidant systems of glutathione peroxidase, catalase and superoxide dismutase enough to neutralize the increased amounts of free radicals formed.
Omega-3 fatty acids are believed to inhibit platelet function and aid the removal of lipoproteins from the body. They are also anti-inflammatory agents by virtue of the fact that they reduce the conversion of arachidonic acid into the inflammatory prostanoids.
Omega 3 is the group of polyunsaturated oils found in fish, soy and flaxseed oils. Eggs are now often fortified with omega 3 fatty acids and are also now added to infant formulas. Omega–8 fatty acids are the monounsaturated oils that are found in olive and canola oils. Omega-6 fatty acids or linoleic acid is found in vegetables and leads to the formation of inflammatory mediators (prostanoids).
Omega-9 fatty acids are the only fatty acids synthesized by the body.
This program recommends olive oil in the preparing of food. Extra virgin olive oil for salads, and pomace oil, which is derived from the pit of the olive for high temperature cooking. Olive oil is high in monounsaturated fatty acids (omega-8 fatty acids). Also recommended are macadamia nuts since they also are high in monounsaturated oils.
Monounsaturated oils optimize the LDL/HDL ratio and their inclusion helps prevents coronary heart disease. Monounsaturated fats reduce blood sugar and triglyceride levels.
Alpha-tocopherol (vitamin E) supplements can slow the progression of atherosclerosis. This is because alpha-tocopherol protects the LDL molecule reduces its susceptibility to being oxidized. Maintaining high levels of vitamin E prevents atherosclerosis. Biology of Atherosclerosis
The genesis of atherosclerosis is due to an attack on the lipoprotein that make up the membrane receptors of cells that line blood vessels (endothelium). The initial injury to the endothelial cells initiates a series of molecular events culminating in the proliferation of fibrous tissue in the arterial wall.
The injury is exacerbated by the inflammatory prostaglandins and a consequential monocyte migration to the injured site. The attachment of monocytes (inflammatory cells) to the injured site produces free radicals, which then attack other cells. Injury to the endothelium results from a variety of factors including tobacco smoke, turbulent blood flow, hypertension, cholesterol and oxidized lipoproteins. The most serious conditions develop in the small arteries of the heart where blood flow is critical to proper heart function.
Pharmaceutical therapy is needed when the flow of blood is obstructed. Despite claims to the contrary, this is not a method of prevention. It is a treatment. Exercise and antioxidants are the most reasonable and best methods to limit atherosclerosis and coronary heart disease. Exercise and a colorful diet can prevent the initial assault on the endothelial cells or minimize their harmful effects, thus keeping their arterial lumens open for the duration of their life. Endothelial membrane receptors that are chemically altered by free radical attack become damaged.
Due to the nature of cell membranes, this local injury leads to widespread membrane dysfunction and an increased permeability to substances from the blood. This alteration in membrane permeability stimulates growth and inflammation resulting in the formation of small blood clots. In addition, the altered permeability of the endothelial membrane increases the stickiness of cells.
Platelets adhere or stick to the injured endothelium to form small clots. Platelets then release growth factors, which further stimulates the atherosclerotic lesion to grow. The attached platelets release thromboxane, a potent vasoconstrictor, other pro-inflammatory agent and mitogenic (growth) agents. These compounds causes the proliferation and deposition of new tissue provoking an excessive inflammatory response, which transforms the site into a ticking time bomb.
Unfortunately, the lumen of an artery like that of a joint surface is not a site that is conducive to inflammatory healing. The resulting attempt at repair further deteriorates blood flow just as the inflammatory response hinders joint function in arthritis. These are the predominant features of atherosclerosis, which posse a serious threat to health. Receptor Involvement in Atherosclerosis Due to the release of growth factors in response to the initial injury to the cells that line blood vessels and elevated lipid levels, there is a dramatic increase in the number of membrane receptors produced. They are formed to aid the removal of lipids.
The binding of LDL is required for removal of cholesterol from blood. Injured cells stimulate an increase in production of the number of low-density lipoprotein receptors. These receptors and the lipoproteins they bind with, are thus exposed to a hostile molecular environment where they quickly undergo lipid peroxidation by free radicals. Therefore by altering the normal receptor responsible for LDL-cholesterol’s removal from the blood, the concentration of LDL in the blood increases.
Unbound LDL-cholesterol is therefore subject to further attack by free radicals and becomes engulfed by scavenger macrophages or foam cells. Foam cells continue to migrate and cause the release of more growth factors, platelet aggregating agents, and other mediators of inflammation. This is the inflammatory process at its most destructive worst. Left unabated, the response to endothelial cell damage will completely clog small blood vessels like those in the heart, shutting off circulation to cardiac muscle. Pharmaceutical Strategies Lipoproteins transport lipids and cholesterol through the bloodstream. An excess of low-density lipoprotein (LDL) is known to increase the risk of developing heart disease. Plaques (atheroma) in the coronary arteries can partially occlude one or more vessels causing heart disease. When a vessel subsequently ruptures, it provides material that acts as a seed, and initiates the formation of clots (thrombosis).
Pharmaceutical therapy uses drugs to alter lipid profiles or enhancing the non-stickiness of platelets. Thrombosis prevention is based on a daily of aspirin. Aspirin is a non-steroidal anti-inflammatory drug that interferes with the cyclooxygenase (both COX-1 and COX-2) enzyme. Plaque formation is associated with the risk factors, cigarette smoking, hypertension, hyperglycemia, obesity, physical inactivity and increased cholesterol or LDL. Many steps in the atherogenic process are targeted as potential areas to attack. The pharmaceutical approach has centered on increasing the synthesis of high-density lipoproteins (HDL) and expediting the removal of LDL by the liver.
Pharmaceutical drugs known as statins (Crestor, Lipitor, Pravachol and Zoloft) act via these mechanisms.