Given our nation’s obsession with cholesterol, I expect the manufacturer of the “monitor your cholesterol at home” appliance to do quite well. Sales should be brisk, as health conscious individuals will want to obtain this latest technological marvel. I shall not be one of them, however.

Frequent monitoring of one’s cholesterol level is an exercise in futility. The home cholesterol monitor is being promoted in the same manner as a home blood sugar monitor for diabetics. The need to closely watch blood cholesterol numbers does not match the importance of monitoring sugar levels, however.

Blood sugar in diabetes is extremely labile. It can change dramatically in a matter of minutes, and it can pose an immediate threat to one’s well being if too high or too low. Total cholesterol levels are very stable, change little over time, and, unless they are low, have no direct relationship to either short-term or long-term health.

When I first wrote about the myth that elevated levels of cholesterol cause heart disease I was cautiously optimistic that the truth about cholesterol would gradually leak into mainstream publications. Unfortunately, the fable has become more firmly entrenched in American medical lore with each passing day.

To dare to suggest that total cholesterol levels are of no value in determining one’s risk of having a heart attack is to risk being viewed as someone who believes that the earth is flat and that the lunar landings were staged on a Hollywood studio set. Nevertheless, an analysis of the medical literature reveals that total cholesterol levels are of almost no value in predicting an individual’s risk of developing atherosclerosis or experiencing a heart attack or stroke. As many people with a total cholesterol number below 200 have heart attacks each year as people whose cholesterol number is over 300.

To appreciate why total cholesterol levels are of little value in determining heart disease risk it is helpful to understand the conditions that do lead to hardening of the arteries, coronary artery disease, and stroke. Two factors must be present if a plaque is to develop in an artery. If either is missing, no plaque will form. One is the presence of oxidized (damaged) LDL cholesterol. The other is damage to the arterial wall.

LDL cholesterol, the so-called “bad” cholesterol, is harmless in its native state. It is not only harmless, it is essential to health as it is a fundamental building block of hormones and other essential body chemicals. Lowering cholesterol levels can lead to depression and sleep disturbances as the body loses the ability to manufacture optimum levels of chemical in the brain.

Heart disease is not caused by elevated total cholesterol levels. It is not caused by elevated levels of LDL cholesterol nor by low levels of HDL cholesterol. It is caused by the presence of oxidized LDL cholesterol.

Oxidation is the name given to the chemical reaction that occurs between oxygen and other molecules. Oxidation is one of the most common chemical reactions in our environment. As ultraviolet rays pass through our atmosphere they strip electrons from oxygen molecules. These unbalanced oxygen molecules, called free radicals, are extremely reactive, attaching themselves to any available substance. Oxidation causes metals to rust, car finishes to whiten, curtains to deteriorate and pictures to fade.

With each breath we take in oxygen free radicals. These free radicals attack cells and molecules throughout our body. LDL cholesterol is one of their favorite targets.

Our immune system has cells called macrophages that are designed to engulf foreign substances when they are encountered. Just as a metal object rusts and changes appearance when it is oxidized, LDL is changed in appearance when it is attacked by a free radical. Once LDL cholesterol has been oxidized and changed in appearance, macrophages view it as a foreign substance to be engulfed and removed from circulation. As an oxidized LDL molecule passes by a macrophage grabs it and pulls it into the wall of an artery forming a foam cell, the first stage of an atherosclerotic plaque.

If no oxidized LDL is present in the bloodstream no plaques will form. The more oxidized LDL present, the greater the risk of plaque formation leading to heart attacks, strokes, and other challenges.

A very interesting study was published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology in 1998. It looked at the risk of coronary artery disease in heart transplant recipients. Total cholesterol, HDL, LDL, and oxidized LDL levels were checked at the time that hearts free of coronary lesions were implanted.

Later, when some of the heart recipients began to experience coronary artery disease, the test results at the time of transplant were reviewed. The investigators found no correlation between levels of total cholesterol, LDL cholesterol, HDL cholesterol, or triglycerides and the development of coronary disease. Likewise, no relationship was found with the use of cholesterol lowering medications. The researchers found that subsequent coronary disease could be accurately predicted only by looking at oxidized LDL levels, which were strongly and directly linked to the formation of new coronary lesions. Subsequent studies have confirmed the finding that oxidized LDL cholesterol is strongly related to the development of coronary artery disease.

Unfortunately, levels of oxidized LDL, which is directly linked to coronary disease, are almost never checked outside of research settings. Yet a device is available for home testing of total cholesterol, which bears no direct relationship to the risk of disease. It appears that cholesterol testing is driven by the pharmaceutical industry. Three of the top ten grossing drugs in the United States lower total cholesterol, but no drug is available to lower levels of oxidized LDL cholesterol.

One of HDL cholesterol’s functions in the body is to protect LDL cholesterol from oxidative damage. This explains the tendency for coronary artery disease to rise as LDL/HDL ratios increase. Studies show that a LDL/HDL ratio of 3.5 represents an average risk for coronary disease.

This means that one HDL molecule is capable of protecting 3.5 LDL molecules from free radical damage. When more than 3.5 LDL molecules per HDL molecule are present, oxidized LDL levels will begin to rise. Therefore, LDL/HDL ratios provide an approximation of the amount of oxidized LDL present in circulation.

Most women have high HDL levels. This means that their risk of coronary artery disease based upon the presence of oxidized LDL cholesterol can be low despite “high” total cholesterol and LDL cholesterol numbers. I have seen women with total cholesterol levels over 300 with LDL/HDL ratios of as low as 2.6. These individuals are at low risk for atherosclerotic disease on the basis of cholesterol, yet they are routinely advised to take cholesterol-lowering medications. People with low LDL/HDL ratios cannot improve their heart disease risk by lowering their cholesterol numbers. They can only expose themselves to the short-term side effects and long-term risks associated with the medications.

There is abundant evidence that individuals with high LDL/HDL ratios can protect themselves by taking optimum amounts of antioxidant nutrients on a daily basis. Studies quoted by opponents of nutritional supplementation to support their contention that antioxidants are ineffective in preventing atherosclerosis are characterized by one of two design errors. In most cases both errors are present.

One error is to use a single antioxidant nutrient. Since the body’s antioxidant defense mechanism requires many nutrients to function properly, single nutrient studies are designed to fail. The other error is to use sub-optimal amounts of antioxidant nutrients. Although 300 to 400 IU of vitamin E is necessary to lower levels of oxidized LDL cholesterol, medical studies typically use only 30 to 100 IU. One would not expect to see any significant change in heart attack incidence with this level of supplementation and this is precisely what the studies demonstrate.

A comprehensive vitamin and mineral supplement along with a phytochemical supplement will provide excellent protection against LDL oxidative damage. While nutritional supplementation benefits everyone, it is life-saving in the case of individuals with high LDL/HDL ratios.

While elevated oxidized LDL levels increase one’s risk of developing atherosclerosis, a second factor must be present if plaques are to develop. The intima, the interior lining of arterial walls, must be damaged. Macrophages are not present when the intima is intact. When it is damaged, however, macrophages appear as part of the body’s attempt to heal the injury.

There are currently three known causes of arterial wall damage. These are cigarette smoking, low-grade infections, and elevated homocysteine levels.

Tar, nicotine, and other substances that are introduced into the bloodstream through tobacco smoke injure the lining of arteries. This places smokers at higher risk for atherosclerosis and associated diseases. Whether or not they actually develop heart disease will depend to a great extent upon how much oxidized LDL is present in their bloodstreams.

One of the theories of heart disease that has gained prominence over the past several years is the chronic infection theory. It is known that people who have evidence of chronic inflammation as demonstrated by “markers” such as C-Reactive Protein are more likely to develop atherosclerosis.

This should not be surprising. When bacteria and other microorganisms enter the bloodstream they are capable of attaching to arterial walls. The immune response to these organisms attracts macrophages to the site where they go to work removing foreign substances, including oxidized LDL, from circulation.

I wrote about the importance of homocysteine in the February 2004 issue of this publication. Homocysteine is an amino acid that is produced when another amino acid, methionine, is used to repair DNA damage within the body. In the presence of B-vitamins and minerals such as magnesium homocysteine is converted back to methionine so that the repair process can continue.

When nutrient levels are low or when a genetic defect prevents efficient conversion homocysteine levels rise. Since homocysteine is toxic to the arterial lining the incidence of heart attack rises 35 percent for every 3 point rise in homocysteine level.

Levels of homocysteine less than 7.2 are generally considered safe. Unfortunately, since the average homocysteine level in the United States is 10, many laboratories consider homocysteine levels of 10 to 13 “normal” despite the 35 to 70 percent increased risk of heart disease these levels represent.

While commercial tests for homocysteine exist, physicians rarely request them. In my opinion, the only way to explain the nearly universal measurement of meaningless cholesterol levels and the lack of highly significant homocysteine testing is the availability of cholesterol-lowering drugs and the lack of drugs to lower homocysteine.

The only way to lower homocysteine is by nutritional supplementation.  I formulated HCY Formula to address this challenge.  Three capsules twice daily is the starting amount.

Despite years of obsessive focus on cholesterol levels, coronary artery disease remains a major cause of premature death and coronary bypass grafts continue to be one of the most common surgical procedures performed in the United States. Given what is known about how plaques form heart disease should be a rarity.

If oxidized LDL cholesterol is present but arterial walls are smooth, plaques will not form. The reverse is also true. If arterial walls are damaged but no oxidized LDL cholesterol is present atherosclerosis will not develop. Both factors must be present for disease to develop.

Both of these disease-promoting factors can be addressed successfully. Oxidized LDL levels and arterial wall damage can be prevented or reversed by avoiding tobacco use and taking safe and effective nutritional supplements.