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Vitamin C Therapy
In Cardiovascular Disease
Michael Lam, MD, MPH www.DrLam.com
(READING
TIPS: For fast reading, scan through the topic headings in BOLD BLACK,
important conclusions in BOLD BLUE,
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the respective LINKS in the Contents.)
| Before You Begin
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. |
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.
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