I don't have any questions, I just wanted to thank you for bringing life back to me.
I was so sick and now I am feeling as good as I did twenty years ago! It has been a long battle: no energy, aches and pains going from one
Dr. to the next. They told me it was anything from arthritis to depression; they had me on steroids for three years... All behind me now!
I just don't know how to thank you. I think it would be wonderful if you could just be everywhere with your caring heart. Information and the
real reason behind all of the bad, sick days that so many of us have had.
Sincerely, Jessica...@telusplanet.net
More
Table of Contents
Reading Tips:
For fast reading, scan through the topic headings in BOLD BLACK, important conclusions in BOLD BLUE, and "Must Know" in BOLD RED. To jump to specific sections in this article, click on the respective LINKS in the Table of Contents.
Information presented here is for general educational purposes only. Each one of us is biochemically and metabolically different. If you have a specific health concern and wish my personalized nutritional recommendation, write to me by clicking here.
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.