Dr. Rath’s discovery reveals that the development of atherosclerotic deposits in the arteries of the heart is triggered by a long term deficiency of vitamin C in the cells building the artery wall as countermeasure to loosening of the endothelial barrier function. Multiple pathomechanisms that lead to clinical manifestation of cardiovascular disease (i.e. lipoproteins deposition) are primarily defense mechanisms aiming at the stabilization of the vascular wall structure.
Ascorbate deficiency is the precondition and a common denominator of human cardiovascular disease (CVD)
Premature CVD is essentially unknown in all animal species that produce high amounts of vitamin C (ascorbate) endogenously. The genetic mutation that rendered all human beings today dependent on dietary vitamin C is the universal underlying cause of CVD. The development of this condition resembles scurvy when a lack of vitamin C and resulting from it failure in collagen production, increases permeability of blood vessel walls resulting in perivascular bleeding. Today, our average diet provides enough vitamin C to prevent scurvy, but not enough to guarantee stable artery walls. As a consequence of suboptimal vitamin C supply, millions of tiny cracks and lesions develop in the artery walls. Subsequently, cholesterol, lipoproteins and other blood risk factors enter the damaged artery walls to repair these lesions.
With chronic vitamin C deficiency, this repair process becomes continuous leading over the course of many years to the development of atherosclerotic deposits which eventually can cause a blockage of a blood flow resulting in a heart attack or stroke.
This concept answers key questions in clinical cardiology
Why do we get heart infarctions, not nose or ears? Why do we get heart infarctions, not nose or ears?
Two critical factors are responsible for this: structural impairment of the vascular wall due to vitamin deficiency combined with the mechanical stress from pulsatile blood flow in the coronary arteries. It is this unique spot (coronary arteries) only the size of few inches in a 60000 miles long blood vessel pipeline where weakness of the vascular wall is exposed first....hide content
Why high blood cholesterol can’t be a primary cause of heart disease? Why high blood cholesterol can’t be a primary cause of heart disease?
If high cholesterol in the bloodstream would cause damage to the arteries it would clog blood vessels everywhere, not just at one predominant spot with the length of only one billionths of the total vascular pipeline. This becomes self-understood if we refocus our attention from the systemic factors in the blood towards the only one relevant target: the stability of the vascular wall....hide content
Why do we get athero-sclerosis, not veno-sclerosis? Why do we get athero-sclerosis, not veno-sclerosis?
The high cholesterol or infection theories would inevitably lead to clogging of veins and capillaries The vitamin C (scurvy) heart disease connection provides the only logical answer to this phenomenon....hide content
Why people get heart attacks, but animals don’t? Why people get heart attacks, but animals don’t?
Bears and other hibernators can reach blood cholesterol levels of 600mg/dl, but are not consider being at risk of getting heart attacks. Animals produce vitamin C internally in amounts from 1g to 20 grams daily compared to human body weight. These amounts are obviously sufficient to optimize the stability of their vascular wall and do not require cholesterol-lowering medications....hide content
Why many heart disease risk factors, such as diabetes, high cholesterol, or high homocysteine levels are connected to vitamin C deficiency? Why many heart disease risk factors, such as diabetes, high cholesterol, or high homocysteine levels are connected to vitamin C deficiency?
The common denominator of these metabolic disorders can be found as they provide compensatory stability for the vitamin deficient wall or relate to vitamin deficiency. This may also be a reason why ascorbate deficiency increases fibrinogen and thromboxane (clotting factors) levels while decreasing endothelial derived relaxing factor (NO0 and prostacyclin....hide content
Which nutrients are important for vascular wall stability? Which nutrients are important for vascular wall stability?
Dr. Rath’s discovery identified that atherosclerosis is nature’s plaster cast for weak and cracked arterial walls that are chronically deficient in vitamin C and other essential nutrients. One of these essential nutrients is the amino acid lysine. Lysine is called an essential amino acid because, similar to vitamin C, it cannot be produced in the human body. Lysine, together with another amino acid, proline, are important components of collagen and their hydroxylation is responsible for optimum stability and structure of collagen fibers. These two amino acids comprise about 25% of all amino acids in the collagen molecule. A deficiency of lysine and proline can also trigger blood vessel wall weakness and instability....hide content
This discovery provides scientific basis for designing effective preventive and therapeutic approaches for heart disease. Modern approaches to heart disease need to refocus from ‘too high’ cholesterol in the blood to “too little” vitamin C and other natural components essential for the production of collagen, elastin, and other reinforcement molecules in the body.
This groundbreaking discovery in heart disease should be taught in every medical textbook and school. It also explains why other cardiovascular conditions, including heart failure, irregular heartbeat, high blood pressure and circulatory problems in diabetes, occur in the case of long-term vitamin deficiencies.