The notion that total blood cholesterol level alone is the key determinant of cardiovascular heath should be dispelled. Polar bears, for example, maintain a total blood cholesterol of over 400 mg/dl and they seldom develop heart attacks. There is obviously a lot more to learn about cholesterol and its link to cardiovascular disease that we currently know.
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 food such as processed fat and 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 PUFA, trans fat frequently used in fried foods, margarine and cooking oil, and oxidized cholesterol from commercially prepared food. In the event that dietary fat and oil is retrieved from fresh, whole and unprocessed food, no lipid peroxidation will take place and 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 resereach 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 is exceeds what is needed.
The total circulating cholesterol therefore remains relatively constant at 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. In fact, a low total cholesterol level (below 150 mg/dl) has been linked with an increased cancer and stroke risk.
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 speeded 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 PUFA 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 amount 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 fat 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 cause 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 fat to our diet exceeds 40 percent.
Some of the natural cholesterol produced by the liver in response to free radical damage is converted into LDL cholesterol and its relative lipoprotein(a) ( Lp(a)). While LDL cholesterol maybe known as the “bad” cholesterol, Lp(a) is even worse. Lp(a) is a plasma lipoprotein that structurally resembles LDL, but with an additional adhesive protein. Lp(a) is also made in the liver and transported to the cell. Studies have shown that Lp (a) holds fast to damaged blood vessel, attracting other Lp(a) molecules, and finally constituting the athrosclerotic plaques. In fact, a high Lp(a) level (more than 30 mg/dl) has been revealed to carry a 10 times greater risks for heart disease than LDL cholesterol level. Lp(a) level should be part of a routine blood screening test for cardiovascular disease risk.
Lp(a) , according to Drs. Pauling and Rath, is the body’s way of repairing its damaged vessel wall that has micro leakages caused at least in part by free radical damage and vitamin deficiencies (more specifically vitamin C ). Humans do not make any endogenous vitamin C and have no self-repair mechanism of the vascular system. Lp(a) is used by the body as a surrogate vitamin C, so to say. Lp(a), unfortunately, has a sticky characteristic and adheres to each other, forming an atherosclerotic plaque over time. The body, at the interim, is unaware. As long as the damage persists due to free radical presence (either from improper diet, aging, pollution, lack of vitamins, or toxins), the body responds by making more cholesterol endogenously in the liver, feeding a viscous cycle of ever increasing Lp(a).
How Much Cholesterol Should You Take?
A low total serum cholesterol level is undesirable for the healthy person. It is very difficult to lower cholesterol only without other types of fats because they are often found intermingled with each other in food. While SFA from animal and diary products is not subject to lipid peroxidation, all animal fats contain some PUFA and cholesterol, both of which undergo auto-oxidation. Those who are serious in reducing total serum cholesterol level should refrain on intake of lipid peroxide-containing fats (trans fat such as margarine) with resulting reduction of free radical pathology. Like trans fat, oxidized cholesterol should be limited as much as possible.
Low fat diet may actually bring harm to health. The correct way is to discern the right type to take and those to avoid. The overall fat intake as a percentage of dietary calories should not fall below 30%. To have plenty of “good” MUFA like olive oil, seeds, nuts and cold-water fish that have high N3 content. Saturated fat is necessary for good health. It should come from free-range poultry or beef, and organic eggs. It is very important to avoid “bad” trans fat, like margarine and fried foods. Moreover, the use of processed PUFA such as corn, saffloweror sunflower oil should be restricted.