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The fundamental and direct answer to your question is: The disease atherosclerosis results in at least one arterial plaque in an artery, but it almost always results in multiple arterial plaques in multiple arteries. Oxidized vLDL (very Low-Density Lipoprotein) and LDL cholesterols are what cause a plaque to form in the first place, and as time passes, additional cholesterol and other lipids (triglycerides, fats and fat derivatives) accumulate within the cells that make up the arterial walls thus narrowing, or "clogging," the arteries.

In the beginning, an arterial plaque is caused when a sufficient number of oxidized vLDL and LDL cholesterol particles embed themselves in the same general area of an arterial wall and cause a cascade of events, starting with an immune response to the artery's injury. In the vast majority of people who have atherosclerosis, a newly-formed plaque evolves over four or more decades; gradually accumulating dead macrophages (a type of white blood cell that is part of the immune system), lipids, calcified layers, and layers of fibrotic material. In persons with the disease hypercholesterolaemia, who suffer from exceptionally high cholesterol levels, plaques develop and thicken at a much greater rate.

The primary layman's term for atherosclerosis is "hardening of the arteries" since the arteries gradually become stiff, rough and misshapen rather than pliable, smooth and straight or gently curved.

I thought that it was important for you to know that what clogs an artery is not only made of cholesterol, therefore what follows is some selected additional information on arterial plaques: The constituents of a mature arterial plaque may not even be half cholesterol. Some of the additional constituents were mentioned earlier, but a more complete and specific list includes phospholipids, dead and living smooth muscle cells (that make up part of an arterial wall), a large specialized protein that is part of every vLDL and LDL cholesterol particle, blood platelets, fibrin and red and white blood cells snared in the cross-linked fibrin net. In general, the more of the lumen that is blocked, the lower the fraction of cholesterol contained in the arterial plaque. Also, the ratio of cholesterol to the other materials contained in a plaque varies from one plaque to another, even in the same person, and from person to person. Another reason for the variance is that different amounts of oxidized cholesterol become embedded in an arterial wall before the cascade of events occurs that ultimately results in formation of an arterial plaque.

I want to make it clear that I am not a medical doctor, and more importantly, I have not even played one on TV. But, I truly did earn a Ph.D. in chemical kinetics. Knowledge is not the most important thing gained from obtaining a Ph.D. What is, is learning what questions must be answered in order to solve or understand the problem at hand. With respect to atherosclerosis, the most important ultimate question is: What can one do to minimize their risk of developing an arterial plaque in the first place? The answer to this question can probably only be answered completely after the answer to other questions are known. A lot of the risk factors for developing atherosclerosis are known; perhaps all of them. Therefore, it is logical that we begin looking for how to prevent, or at least how to slow the progression of, atherosclerosis by eliminating as many risk factors as possible. It appears that things can only go downhill once a plaque has formed, however the human body does have an amazing ability to heal itself, hence it is my opinion that it is possible to prevent, and even reverse, atherosclerosis in most people provided that the disease has not progressed too far.

I believe that the three most important facts yet known about atherosclerosis are: 1) Only vLDL and LDL cholesterol particles become stuck to and then embedded in arterial walls. 2) Only oxidized cholesterol molecules are found in the arterial walls; and 3) when the density of oxidized cholesterol in an arterial wall reaches some magic number, the eventual result is a very damaging immune response. These three facts lead to the four most important preliminary questions, the answers to which must be known in order to answer the ultimate question: 1) Do only vLDL- and LDL cholesterol particles containing oxidized cholesterol penetrate and embed in an arterial wall? Or 2) Is the cholesterol in the particles oxidized after they penetrate and embed in an arterial wall, or do both 1) and 2) occur? 3) Can powerful antioxidants such as vitamin C, lipoic acid, eugenol, natural mixed tocopherols (d,α-, d,β- and d,λ-tocopherols), or other natural and safe antioxidants chemically reduce some forms of oxidized cholesterol back to cholesterol?

For the time being, I take 1000 mg of vitamin C and 200 mg of lipoic acid twice a day for their well-known powerful antioxidant and radical scavenger abilities. Since I am not any reader's doctor, I am not recommending that anyone take these two supplements, and there is one Warning! Anyone taking any medication, including insulin, for high blood sugar, it is very important that he or she does not take lipoic acid without speaking to his or her doctor first. I do recommend that the reader never consume any food that contains "partially-hydrogenated [name of oil]" since all of those modified oils contain trans fats, which are known to raise the LDL cholesterol of almost everyone. One should also never heat olive oil and other oils that contain a high percentage of unsaturated oils above approximately 350 ˚F because doing so will convert some of the [naturally-occuring] cis double bonds to transdouble bonds. This means that one should not stir fry with olive oil and other "delicate" oils. Lastly, I strongly recommend that cooks do not heat oils to the point that they smoke. Any oil that is smoking is being oxidized and is hot enough to form trans double bonds. Use fat, not oil, if a pan needs to be that hot. Coconut fat, palm kernel fat, and beef tallow are much healthier alternatives to oils that are heated to the smoking point.

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Q: What is it called when arteries get clogged with cholesterol?
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What do you call a person whose arteries to the heart become clogged?

A person whose arteries to the heart become clogged has a cholesterol.


Can eating cornstarch give you clogged arteries?

No. Clogged arteries are caused by too much 'bad' cholesterol and triglycerides in your blood...nothing to do with cornstarch.


Can too much cholesterol lead up to clogged arteries?

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There are several disorders that can lead to clogged arteries. These include but are not limited to: high blood pressure High cholesterol diabetes...


Can skinny people get clogged arteries?

Yes, too much cholesterol will clog them.


The build-up of cholesterol on the walls of the arteries is a condition known as?

Arteries maybe clogged by fatty deposits on their walls causing the condition known as Atherosclerosis.


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What tends to lower the level of cholesterol in the blood?

A major reason for wanting to lower your blood cholesterol is to stop it from clogging your arteries. Clogged arteries can lead to health problems and heart problems.


Which statement is not true?

The body does not make enough cholesterol.


Can high cholestrol kill you?

Yes, it is called clogged arteries aka a heart attack.


What delivers the cholesterol that contributes to plaque formation in the lining of the arteries?

LDLs ( low density lipoproteins) that's why the cholesterol in combination with LDLs is called " bad cholesterol".


What is a waxy fat-like substance that can build up in the arteries?

Cholesterol is a waxy fat-like substance that can build up in the arteries.