Atherosclerosis, a thickening or narrowing of the arteries that leads to a heart attack or stroke, has become a common medical problem. This website is intended to allow you to become an informed patient who can manage his or her own care, ask the right questions, insist on adequate management and information, and seek an optimal outcome for herself or himself. Perhaps it will even help the health professionals who are giving care to better understand and, hopefully, incorporate into their practice the nutritional approach to this serious, degenerative cardiovascular disease.

The status of cardiovascular health is regulated by endothelium - the innermost lining (layer) of arteries. The endothelial cells control the elasticity - relaxation and tightening - of blood vessels (the more elastic the arteries, the better).

However, subsequent dysfunction of the endothelium plays a central role in the process of arterial fatty plaque formation, leading to the development of atherosclerosis.

The endothelial function can be measured now. A relatively new test, called FMD - flow mediated dilation, can be done by stopping blood flow to the lower arm with a blood pressure cuff, releasing it, and measuring the blood vessel diameter of an artery with ultrasound.

In the processs of atherosclerosis then, arterial walls - especially the aorta and the coronary arteries serving the heart - become covered with fatty plaques, called atheromas that keep on enlarging.

Although arterial plaque formation my be triggered by many factors, they all relate to:

• an injury to the endothelium and/or underlying smooth-muscle cells and, therefore,
• an inflammatory process initiated by this injury.

The injury to endothelial cells - the innermost lining (or layer) of an artery, triggers the response of blood cells called platelets to accumulate at the site of injury, in an effort to plug the damaged area.

The sticking together platelets secrete a growth factor that stimulates the outgrowth of underlaying endothelial cells. These cells then begin to protrude into the arterial wall.

Through specific receptors, the outgrown endothelial cells:

• ingest lipoprotein particles and
• accumulate cholesterol and triacylglyceroles (triglycerides), transforming themselves into plaque - fat-engorged foam cells.

Finally, connective tissue penetrates the plaque, which in advanced situations can become calcified and, consequently, add rigidity to the blockage (occlusion).

Atherosclerotic plaque formation is an overly aggressive homeostatic process in order to correct and balance the condition triggered by the arterial endothelial injury. This process occurs as long as there is a presence of platelet accumulation function.

There is one kind of harmful, oxidative agents of significant importance that initiate the endothelial injury leading to atherial plaque formation, called free radicals.

	Free radicals, also called reactive oxygen species (ROS), are highly unstable molecular fragments - both of internal and external origin. They are being constantly released in the body, whenever we are exposed to harmful, both dietary and environmental factors, such as

• drugs (of all kinds)
• chemicals (pesticides, herbicides, insecticides, etc.)
• processed and irradiated foods
• food additives and preservatives
• artificial food colourings
• polyunsaturated, mainly vegetable oils, and rancid oils
• tap water
• tobacco
• excessive, prolonged stress, etc.

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As our cardiosvascular system is highly susceptible to free radical damage, antioxidants are of incredible help here. By neutralizing and "mopping up" free radicals in the body, antioxidants play a key role in slowing down the process of atheromatous plaque formation.

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