04-13-2008, 01:05 PM
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#7
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Status: Ultra Moderator
Join Date: Jun 2007
Posts: 1,652
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Quote:
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Originally Posted by Dinoiii
I am not exactly certain what sort of information you are looking for. There were an array of very biased presentation show in that video stream. For instance, even the basic classification of cholesterol as minimally a "protein" while partly accurate is mildly distressing. The truth be told, cholesterol is a waxy substance consisting of fats (lipids - hence, why you would obtain a "lipid" panel) AND proteins ... the so-called "lipoprotein." The speakers immediate dismissal of the lipid component was an almost immediate turn-off for me. It became more clear why when Mercola got on at the end to talk about his "Inner Circle" (which comes with a fee mind you, and you can get all this great stuff - YAWN!).
Another questionable notion is even the breakdown of "good" (HDL) and "bad" cholesterol. That particular nomenclature has NOTHING to do with things being carried to and from tissues. With someone discussing the "oxidation" potential, it must be clear that it is LDL that carries the oxidized particulate matter - hence, its proclamation of "bad."
There is a clear association with statin drugs and reduced morbidity/mortality when co-administered with various pathophysiologic states. This is not by chance, but I DO agree that it is likely NOT the effect on lowering cholesterol that holds pertinence and very rarely would I recommend a statin drug (hence, my personal propaganda against red yeast rice as well - but this has been spattered all over this forum). There is alternative hypothesis that in addition with working to combat HMG-CoA reductase (this is the quintessential enzyme in cholesterol synthesis by the liver), there are also anti-inflammatory properties associated with these drugs.
As for heart disease (in particular), 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. One thing that crops into my mind, however, is volume of distribution data which too seems to be disregarded by far too many in both the pharmaceutic and dietary supplement industries both.
What I do agree with...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 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 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 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 risk of cancer and stroke.
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 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 fat to our diet exceeds 40 percent.
I could go on all day about this and have written various articles across the internet as well - if searching hard enough, you can always find them.
D_
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Good info from dino 
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