The past 30 years saw more and more people opting for the use of mega-dose Vitamin C therapy together with lysine, proline, and carnitine to prevent and treat heart diseases. Although this therapy is still not within mainstream medicine, many well-conducted studies have proven the effectiveness of these natural compounds.

We will be dwelling on this subject in greater detail below. Meanwhile, let us first have a basic understanding of the functions of the endothelial and how atherosclerosis, the foundation of cardiovascular disease comes about.

ENDOTHELIUM

We all know that atherosclerosis is the main cause for heart attack and strokes. Atherosclerosis is the result of injury to the extremely thin layer of endothelial cells that line the inside surface (the lumina) of the heart and blood vessel walls. Circulatory toxins such as smoke, free radicals, sugar and infection cause these injuries. Numerous established studies have confirmed that an impaired endothelial function is linked to all major coronary heart diseases.

Although the endothelium is extremely thin, it is a highly complex structure in terms of function. It regulates the structural integrity of the vascular wall by secreting numerous factors that determine not only the contractility of the walls but also the homeostasis of the blood. Imbalance of this contractility function will lead to hypertension. If the local vascular homeostasis is disturbed, it will result in platelet deposition, aggregation and a release of factors that promote smooth muscle proliferation. When this happens, you may get fibrosis, atherosclerosis and thrombus formation. As imbalances are first initiated at the endothelial, where insults excite an inflammatory response, the endothelium is therefore the first link between inflammation and coagulation. The endothelium also represents a surface where proteins are involved in coagulating. It is also here that the development of inflammation are expressed

We will now look at the cascade of events a little closer. A high sugar diet and an environment full of cigarette smoke produce toxins such as free radicals that are ever ready to attack the endothelium. The endothelium, in an attempt to heal itself will launch an inflammatory response to get rid of the unwanted guests.

The characteristics of an inflammatory response are as follows:

1. Vasodilatation to increase blood flow to the area.

2. Increase vascular permeability to allow diffusible components to enter the site.

3. Cellular infiltration by chemotaxis, or the directed movement of inflammatory cells through the walls of blood vessels to the site of injury.

4. Changes in biosysnthetic, metabolic, and catabolic profiles of many organs.

5. Activation of cells of the immune system as well as of complex enzymatic systems of blood plasma.

During an inflammatory response, our blood flow is increased to transport more white blood cells to the injured area. The white blood cells first surround the damaged tissue, then together with the other cells in the damaged tissues neutralize, repair the damage and remove whatever is causing the injury. This reaction can be measured in the blood by the elevation of a substance called C reactive protein.  

 Meanwhile, a small amount of LDL ("Bad") cholesterol that has built up in the artery wall becomes oxidized. Oxidized LDL is one of the triggers that set off a chain reaction. It causes the endothelium to express a special kind of molecule "glue" called ELAMS (endothelial-leukcyte adhesion molecules). These molecules, which happen to be floating by in the bloodstream causes certain kinds of white blood cells (monocytes and T lymphocytes) to stick to the endothelium. At this point in time, the inflammatory response is still well under control and normal, whether it is in the artery or in the tissue.

Beyond this point, the healing process goes off track.The white blood cells will start to move between and below the endothelium and cause damage in two major ways. Firstly, they will cause some of the muscles cells in the artery walls to grow and secondly, they incorporate particles into the artery wall, consuming the oxidized LDL particles. What results from here is a fatty streak that becomes a fibrous plaque.

This intricate process begins in the tissue under the endothelium. Due to inflammatory reactions, the endothelium's structure becomes permeable to lipoproteins, particularly low-density lipoproteins (LDL) and macrophages. These particles will enter into the site of injury, accumulate cholesterol as cholesterylester and develop into foam cells. A raised LDL-cholesterol and related cholesterol carrier called lipoprotein (a) concentration is recognized by many as a major risk factor for heart disease as it appears to be the donor of cholesterol deposited in the artherosclerotic plaque. Being adhesive, the cells will attract other substances, resulting in a continuous deposition of unwanted conglomerate which we called fatty streak. The latter consist of lipids (fats), complex carbohydrates, blood, blood products, fibrous tissue, oxidized ascorbates and calcium deposits. As the fatty streak becomes bigger and bigger, this resulting fibrosis forms an " endothelial tumor" or a plaque. The process of plaque formation is called atherosclerosis. Atherosclerosis blocks the blood's pathway and narrows the arteries over time.

The arteries in our bodies consist of three layers:

1 The intima is composed of the endothelium and underlying sub-intimal connective tissues.

2 The media is composed of the internal and external elastic lamina surrounding the smooth muscles.

3 The adventitia lies at the outer most area comprising of connective tissues in which nerve fibers are dispersed.

Therefore, the hallmarks of an artherosclerotic vessel are intimal hyalinization, medial hypertrophy, and endothelial hyperplasia. Histologically speaking, lipids accumulate in the endothelium and muscle cells. In severe cases, lipid particles appear extracellulary in the intima.

It is very interestingly to note that artherosclerotic plaque contains both oxidized lipids and relatively large amounts of alpha-tocopherol and ascobate. During various studies, researchers have discovered that plaque samples which contained more ascorbate and urate than normal arteries have no discernible differences in the Vitamin C redox status between plaque and control materials. The most abundant of all studied lipids in plaque samples was free cholesterol, followed by cholesteryl oleate and cholesteryl linoleate. The study also noted that approximately 30% of the plaque was oxidized.

If we want to prevent or slow down the accumulation of cholesterol due to the modification or oxidation of LDL, we can take Vitamin C. Various types of heart cells, including endothelial cells, can oxidize the low-density lipoprotein (LDL) form of cholesterol and promote heart disease. As such, taking Vitamin C will help to enrich the endothelial cells and make them less likely to oxidize LDL.