These disorder and Cancer (which are certainiy not the only proliferative disorders) have in common the excessive production of abnormal tissue. In atheroscierosis, abnormal tissue, called "plaque' grows and accumulates inside arteries, eventually disrupting blood flow.

This process changes the internal architecture of the artery. When a plaque ruptures (which happens for several reasons, such as the mechanical stress of hypertension, infection or inflammation), the clot that forms may totally block blood flow (thrombosis), thereby adversely affecting tissues "downstream" from the clot. In the arteries of the heart, this is termed a heart attack, and the death of heart muscle usually results. In the arteries supplying the brain, the phenomenon is called an ischemic stroke.

In atherosclerosis, the build-up of plaque is a multi-step process:

Step 1: Oxidation of LDL particles by free radicals. Circulating particles of fat (LDL or low density lipoprotein-the "bad" cholesterol) must be damaged or oxidized by free radicals (see Mangosteen: The X Factor for a detailed description of the process).

Step 2: Endothelial dysfunction. The inner lining of the artery, the endothelium, inappropriately manufactures "adhesion substances" that trap the damaged LDL particles circulating in the bioodstream and pull them across the artery endothellum.

Step 3: Formation of foam cells. Specialized white blood cells called macrophages ingest the damaged LDL particles. After having ingested many LDL particles, these white blood cells change into "foam cells" and die while still inside the artery wall.

Step 4: Smooth muscie cell proliferation and migration. Smooth muscie cells in the artery wall multiply and grow inappropriately inward in order to encase the choiesterol-containing foam cells in what eventually becomes a fibrous covering.

If this process is allowed to continually occur,it will lead to larger and larger plaques.

Once a plaque is formed, it generally needs to become inflamed in order to rupture and stimulate the production of a clot. Bacteria can infect a plaque and cause inflammation. Usually these bacteria get into the bloodstream from the mouth when periodontal disease exists. As people brush their teeth, irritating and causing the diseased gums to bleed, the disease-causing bacteria then enter the bloodstream.

Additionally, high blood pressure can cause inflammation in a plaque through mechanical irritation from increased flow pressures and turbulence.

The inflamed plaque becomes swollen and soft. It is the softening of its surface layers that can lead to rupture. When the inflamed tissue ruptures, it releases a substance into the bloodstream that triggers what is called the "coagulation cascade."

Once triggered, this chemical cascade produces a fine mesh of sticky strands to which blood platelets stick. These plateiets are the particles in circulating blood that form clots. Platelets can be thought of as the "bricks," so to speak, from which a clot is built.

Clots are intended to stop blood flow so that a hole or a rupture can be repaired without blood escaping from the body or into parts of the body where it shouldn't be. This is what happens on the surface of the skin when we cut or scrape ourselves.

In this case, the clot formed is commonly called a "scab' and it is a beneficial thing. However, if the clotting occurs inside a blood vessel where blood must pass to feed tissues downstream, it can be deadly. "Chemoprotective" or "chemoprevention" are terms that refer to the body's utilization of nutrients to counteract all the steps leading to the formation of plaque and the eventual rupture that causes a stroke or heart attack. The relevant subjects in the research are listed below.

Catechin research on mangosteen has demonstrated the following in the area of atherosclerosis:

• Decreased liver production of LDL and VLDL ("bad" cholesterol)

• Protection of the LDL molecule from free radical damage (antioxidant effect more potent than that of vitamin C)

• Decreased amount of absorption and digestion of dietary fats

• Normalization of endothelial cell function in the artery so that adhesion substances are not formed

• Inhibition of the growth factors that cause smooth muscle cells in the walls of arteries to grow abnormally and form plaque

• Inhibition of bacterial proliferation in the mouth that leads to gum disease and the possible infection of arterial plaque

• Dampening of the inflammatory response, which leads to plaque rupture and triggers the coagulation cascade that produces the deadly blood clot

• Inhibition of thrombin-induced clot formation (the coagulation cascade)

Xanthone research has revealed the following properties:

• Antioxidant activity (surpassing that of vitamin E) that protects LDL particles from free radical damage in laboratory studies

• Antibacterial action to prevent the infection of plaques

• Anti-inflammatory activity capable of danspening the inflammation, which can lead to plaque rupture

Proanthocyanidin research has revealed the following properties:

• Antioxidant activity to protect LDL particles from free radical damage

• Antibacterial effects

• Normalization of endothelial vasodilatory function in the arteries through the increased production of Nitric oxide

• Antithrombotic (anticlotting) effect

• Anti-inflammatory effect to lessen the probability of plaque rupture

• Regulation of adhesiom molecule production by endothehal cells

Sterol research has revealed the following properties:

• Normalization of lipid production to prevent the excessive formation of LDL

Polysaccharide research has revealed the following properties:

• Antibacterial effect