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GSE Atherosclerosis occurs as a result of damage to an ascorbate-deficient blood vessel wall

Why does atherosclerosis occur?

ASCORBATE deficiency leads to arterial wall injury

Vitamin C is used for ongoing tissue repairs - arteries (and every other body tissue) constantly undergo decay, repair, and replacement. Tissue repair and replacement requires a binding protein called collagen, which the body produces from vitamin C (ascorbate). An insufficiency of ascorbate will cause artery walls to form lesions (wounds) as they fall into disrepair.

A chronic deficiency of vitamin C leads to scurvy - eventually the lesions would rupture and you will bleed to death through the artery wall.

Plaque formation is part of a life-saving inflammatory reaction to preserve the integrity of the arterial wall

Atherosclerosis is a damage-control response

. . . to chronic inflammation of the endothelial cells (ECs) lining the arterial wall caused by nutrient deficiencies and lifestyle choices

And NOT by elevated cholesterol and calcium, whose deposits in the arteries are secondary to the primary causes.

The body's “Plan B” for chronic scurvy is to make a scab –   not an ideal plan, but a protective inflammatory reaction that will at least keep you alive long enough to address the prevailing ascorbate deficiency. Lp(a) (a variation of LDL cholesterol) is attracted to the lesions, forming sticky clots, called arterial plaques. Combining with the other normal repair substances the plaque acts as a protective “scab”on a lesion.

Endothelial cells function as a barrier - to prevent toxic substances in the blood from entering the elastic smooth muscle in the middle of the vessel wall. Sensing an injury, ECs immediately initiate steps to protect the integrity of the wall, thereby initiating and promoting the atherosclerotic process:

To avoid a blood vessel rupturing because of chronic injury to the endothelial artery lining - usually as a consequence of:

(a) A lack of antioxidants to control oxidative stress (especially in the presence of heavy metals) - triggered by oxidative stressors often present in a variety of conditions, such as hypertension, cigarette smoking, immune injury, and diabetes;

(b) Mechanical stress - usually in a location under high pressure or turbulence;

And/or

(c) A vessel wall weakened by nutrient deficiencies in the diet, and in particular a lack of vitamin C;

Arterial wall ECs initiate life-saving action to “beef up”the wall with a deposit of an artery-thickening layer of plaque.

The damage irritates /inflames the endothelium causing an inflammatory immune response for the purpose of healing or controlling the damage - This involves a complicated series of steps, including T-cell activation, foam-cell formation, smooth muscle migration, and blood platelet adherence and aggregation.

For more details on the development of atherosclerosis:

Atherosclerosis Process –Overview

Atherosclerosis Process – In Detail

Plaque in your arteries is Saving your Life!

Arteries are repaired with an artery-thickening plaque as a life-saving response to chronic injury, to prevent a person from bleeding to death through a weakened arterial wall (usually under high pressure).

Renowned researchersDrs.Matthias Rath M.D. and two-time Nobel prize winner Linus PaulingPh.D., point out that the deposition of plaque at least allows time for the person to reproduce before his or her eventual death caused by narrowed arteries.

DO NOT REMOVE ATHEROSCLEROTIC PLAQUE UNTIL YOU HAVE DEALT WITH THE CAUSE OF DAMAGE AND STRENGTHENED YOUR ARTERIES

Using cholesterol-lowering drugs (or any other mechanism) to remove cholesterol content from arterial plaque before rebuilding the arterial walls is acting against your body's own survival tactic. If you are not getting enough vitamin C to produce sufficient collagen to maintain the integrity of your arteries, then the atherosclerotic plaque (partly composed of LDL cholesterol) is saving your life! Lowering cholesterol will somewhat reduce plaque build-up, but simply removing plaque without first restoring the artery to health is like tearing a scab off a wound.Your body first needs sufficient vitamin C to heal and strengthen your arteries.

Additionally, you obviously need to deal with whatever is causing the damage . . .

Dr. Linus Pauling, Phd. (1901- 1994) - is one of only two people to receive more than one Nobel Prize, the other is Madame Curie, and he is the only person to receive them unshared. Pauling was one of the first scientists to work in the fields of quantum chemistry, molecular biology and orthomolecular medicine. In this article, he is especially referenced for his work on the involvement of vitamin C and the amino acid L-lysine in heart disease.

What Injures Artery Walls?

Injury to the arterial wall irritates and inflames the arterial lining (endothelium) causing an inflammatory response - damage to the arterial lining can be inflicted by several culprits, including:

–   Mechanical Stress – fluid shear stress generated by high pressure blood flow, usually in arterial branch locations;

–   Oxidative Stress uncontrolled by antioxidants basically the oxidant molecules in your body are outnumbering the antioxidants; highly reactive oxidant molecules can be present in food and water, and produced by the body in response to several factors, including elevated blood sugar levels, toxins, emotional stress, microbial infection and many other triggers. Excess exposure to chlorine, in particular, has been implicated as a predominant source of oxidants:

"Nothing can negate the incontrovertible fact, the basic cause of atherosclerosis and resulting entities such as heart attacks and stroke, is chlorine."

–   Joseph Price, M.D. Author “Coronaries, Cholesterol, Chlorine”

–   Hyperglycemia increases damaging AGEs – glycation is a process whereby sugar molecules are added to lipid molecules or proteins, to form a glycolipid or glycoprotein, and harmful by-products, called AGEs (Advanced Glycation Endproducts). AGEs can directly damage the endothelium; AGEs can be formed in and out of the body. Exogenously, typically when sugars are cooked with proteins or fats.

–   Elevated homocysteine levels in the blood – can be a consequence of high meat and/or dairy consumption

–    Overly acid-forming diet

For more information on how the arterial lining is being damaged:

What injures arteries?

What Weakens the Arterial wall Integrity?

Weak, ascorbate-deficient, vessel walls are more easily damaged by injurious mechanisms

 

Deficiency of vitamin C ascorbate together with the amino acids lysine and proline, maintain arterial structural integrity by their role in forming connective tissue components collagen and elastin.

Weak Walls (Due to chronic scurvy)

CVD - A Simple Cure

Uric acid is also reported to be a possible substitute for Vitamin C - Primates (includes humans) have higher levels of uric acid compared to other animals, Since uric acid is reported to be a moderate antioxidant, this is possibly another substitute mechanism for primates' lower ascorbate levels

Ames BN et al (1981) Proceedings of the National Academy of Sciences USA

Progression Rate in CVD

Atherosclerosis can sometimes progress unnoticed for decades - until its first symptoms and signs appear in the advanced stage, often announcing itself as a "sudden" heart attack.Ultrasound studies demonstrate coronary atherosclerosis exists in 37% of “healthy”heart donors aged 20-29, 60% of those 30-39, and in 85% of those older than 50.

CVD Can Develop from a Young Age

77% of 300 American soldiers killed in Korea, average age 22 years, had gross evidence of arteriosclerosis in the coronary arteries; in several, one or more heart arteries were partly or completely occluded.

Enos WF et al, Coronary disease among United States soldiers killed I action in Korea. J Amer Med Assoc, 1953. Similar findings were reported in American college students, who died in auto accidents

Atherosclerosis can also develop erratically and rapidly - Records involving the photographing of arteries (called arteriography or angiography) as plaque develops in patients showing CVD symptoms, clearly demonstrate that development can also be erratic and develop rapidly in just a few months. A university hospital study in Germany compared slow and rapid atherosclerosis progression in 79 patients with CHD using angiography.

Results indicated that rapid progression was NOT determined by: Age differences, sex, number of vessels diseased, interval between angiographies, smoking, having hypertension or diabetes mellitus, or on serum concentrations of LDL cholesterol, HDL cholesterol, triglycerides, and/or Apo B.

However, it was found that elevated Lipoprotein(a) levels are a clear risk factor for the rapid angiographic progression of coronary heart disease (CHD) - The link between Lp(a) and rapid progression may be the effect Lp(a) has in preventing blood clot dissolution. As typically observed, average Lp(a) concentrations in all patients were higher than in healthy subjects. (Note: The angiographic picture of progressive narrowing may have included the accelerated proliferation of vascular wall cells).

Wolfram Terres, MD et al, Rapid Angiographic Progression of Coronary Artery Disease in Patients With Elevated Lipoprotein(a),Circulation (AHA),1995

Lp(a) –“The Repair Man”

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