Atherosclerosis occurs consequential to injury of a weakened arterial wall

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

Ascorbate deficiency is the primary cause of a weakened wall

Vitamin C (together with the amino acids lysine and proline), maintain arterial structural integrity by their role in forming connective tissue components collagen and elastin.   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 using 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 chronic scurvy.    Eventually the lesions would rupture and you would bleed to death through the arterial wall.

Weak Walls (Due to chronic scurvy)

CVD (related to atherosclerosis) - 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

Various mechanisms can injure the weakened arterial wall

(a)  Mechanical stress.     Usually in a location under high pressure or turbulence;

(b)  A lack of antioxidants to control oxidative stress (especially in the presence of heavy metals).    Triggered by oxidative stressors often present ; Basically the oxidant molecules in your body are outnumbering the antioxidants; highly reactive oxidant molecules can be present in food and water,  produced by the body in response to several factors, including elevated blood sugar levels, toxins (Excess exposure to chlorine, in particular, has been implicated as a predominant source of oxidants:), cigarette smoking, emotional stress, microbial infection, and in a variety of conditions E.g.hypertension, immune injury, and diabetes.

(c) Other causes:

What injures arterial lining?

Endothelial cells (ECs) function as a barrier.   ECs prevent toxic substances in the blood from entering the elastic smooth muscle in the middle of the vessel wall.

Chronic injury irritates /inflames the endothelium causing the ECs to initiate 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 the purpose of depositing an artery-thickening plaque over the damaged area to prevent a person from bleeding to death through a weakened arterial wall (usually under high pressure). This process is called atherosclerosis.

For more details on the development of atherosclerosis:

Atherosclerosis Process -Overview

Atherosclerosis Process -In Detail

Plaque in your arteries is Saving your Life!

Renowned researchers Drs.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.

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.

Fix the wall / Prevent the injuries

Chronic inflammation of the endothelial cells (ECs) lining the arterial wall is caused by nutrient deficiencies and lifestyle choices.    NOT by elevated cholesterol and calcium, whose deposits in the arteries are secondary to the primary causes.

Tools Against CVD

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.

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”