High total serum cholesterol and LDL cholesterol are significant risk factors of cardiovascular disease. 14 million Americans have heart disease and more than 2,600 die daily from heart attacks in the United States alone. 15% of adults in their late 30s to 40s are afflicted by cardiovascular disease, about 50% of 55 to 64 year-olds, and 65% of those will be afflicted in the next decade.

Developed countries have shown a decrease in dietary fat and cholesterol consumption in recent years. This is largely the result of on-going massive public health campaign advocating a low fat, high carbohydrate diet as ideal to bring down blood cholesterol level to prevent arthrosclerosis. Despite this effort, the number of people with elevated blood cholesterol continues to increase. Obviously there are other causative factors that have not being addressed. In America alone, over 40 million prescription was written yearly for cholesterol lowering medications.

After decades of research, nutritionists are still debated on the etiology of high cholesterol and the best way to bring it down. Let us take a closer look.

Cholesterol Basics

Cholesterol is a waxy substance consisting of fats (lipids) and proteins. It is one of the macro-nutrients necessary for life. Cholesterol is made in the liver and is carried in the blood on carrier molecules called lipoproteins. The main lipoproteins categories are very-low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density-lipoprotein (HDL). Once bound to the carrier HDL, the cholesterol is known as HDL cholesterol. HDL in effect transports fat from the cell to the liver. When the HDL cholesterol level is high, it is more cardio protective. Therefore, HDL cholesterol is considered "good " cholesterol. LDL is the carrier of oxidized cholesterol as LDL cholesterol from the liver to cell. Elevated LDL cholesterol is directly correlated with increased cardiovascular risk. LDL cholesterol is therefore called the "bad" cholesterol.

Cholesterol, when unoxidized, is an antioxidant and free radical scavenger in its naturally occurring state. In fact, unoxidized cholesterol guards the cell membranes' phospholipids from free radical damage and protect it against atherosclerosis, cancer, and other free radical attack. Also, cholesterol is a predecessor to many steroid hormones and vitamin D. It is produced at the liver at the rate of 3,000 to 4,000 mg a day.


Cholesterol and Free Radical Activity

While the exact mechanism of how cholesterol affects our body is still under intense investigation, it is clear that the unified theory of free radical damage caused by unhealthy foods such as processed fat and oxidized cholesterol is the most likely mechanism. Free Radical damage to our blood vessels is one of the primary causes of atherosclerosis. The most important cause of free radical pathology is the excessive dietary fat consisting of processed poly-unsaturated fatty acid (PUFA) and trans fat (frequently used in fried foods, margarine, cooking oil, and oxidized cholesterol from commercially prepared foods). In the event that dietary fat and oil is retrieved from fresh, whole, and unprocessed foods, no lipid peroxidation will take place and the cell membrane will remain healthy in a normal cis-configuration without any free radical damage.

One theory advanced by the late Nobel laureate Dr. Linus Pauling, together with his research cohort Dr. Matthias Rath, is that the total serum cholesterol is really an indicator of the amount of free radical damage in the body. Our body maintains an optimum level of total cholesterol level as well as a delicate balance among its subcomponents. A negative feedback mechanism exists within the body that decreases the rate of endogenous synthesis when the dietary intake exceeds what is needed. The total circulating cholesterol remains relatively constant between 170-200 mg/dl for the normal adult. The higher the free radical level, the higher the body needs to produce cholesterol internally from the liver to act as an antioxidant and free radical scavenger. Cholesterol level is therefore an indicator of free radical activities in the body.

Free radicals are not all bad. Some of them are definitely necessary to protect us against cancer cells and infections. In fact, a low total cholesterol level (below 150 mg/dl) has been linked with an increased risk of cancer and stroke. Too many free radicals, on the other hand, is detrimental to our health.

Cholesterol in its natural state is therefore actually good for us. During commercialization, lipid (including fat and cholesterol) peroxidation takes place as soon as fats and oils are extracted from the foods in which they naturally occur. This commercialization process is sped up by metallic ions, particularly iron and copper. Extensive lipid peroxidation can occur without an apparent stale or flavor, like in peanut butter, the making of salad and cooking oil, and also in so-called cold-pressed oils. During the processing of PUFAs to make cooking oil, rapid peroxidation can take place and free radicals are released. This process is accelerated by heat, atmospheric oxygen, light, and trace amounts of unbound metallic elements.

Oxidized cholesterol is a free radical generator. It is attached particularly to low-density lipoproteins as LDL cholesterol as it goes from the liver to the cell. Hamburgers and other cooked and processed foods contain animal fats that are usually high in oxidized cholesterol when cooked. Foods cooked in animal fat and fried in processed PUFA (such as corn oil) also have high oxidized-cholesterol content. As a result, the higher the LDL cholesterol level, the higher the risk of cardiovascular disease. Research has shown that rabbits that consumed a small amount of oxidized cholesterol for merely 12 weeks had atherosclerosis plaques that were two times as big as the control population. Studies reveal that heart attack risk falls 2% for every 1% drop in LDL cholesterol level.

One of the most important causes of free radical pathology is the excessive dietary fat consisting of processed PUFA or trans fat frequently used in fried foods, margarine, and cooking oil. In the event that dietary fat and oil is retrieved from fresh, whole, and unprocessed food, no peroxidation will take place and cell membrane will remain healthy in a normal cis-configuration without any free radical damage. Studies have shown that 20% of dietary calories as commercially available fat will not surpass the control threshold of endogenous free radical protection. Unfortunately, the current contribution from such commercially processed fat to our diet exceeds 40 percent.