Vitamin C and Heart Health: Dr. Rath’s Theory of Cardiovascular Disease
Did you know that chronic deficiency of vitamin C can cause heart disease? It is widely known that you need sufficient amounts of vitamin C to prevent scurvy. But the work done by Dr. Matthias Rath and his fellow researchers supports the concept that vitamin C deficiency is an independent risk factor for atherosclerosis (plaque deposition along the arteries) and cardiovascular disease.
In a ground-breaking 2015 study published in the American Journal of Cardiovascular Disease, researchers from the Dr. Rath Research Institute showed that it is not cholesterol but chronic deficiency of vitamin C that leads to atherosclerosis – the primary cause of heart attacks and strokes – which is characterized by hardening and narrowing of the arteries.
Traditional versus new theory of cardiovascular disease
According to conventional thinking, elevated LDL levels in the blood damage the endothelium – a thin layer of cells that line the interior of the blood vessels. What follows is a series of immune and inflammatory responses in the endothelium that trigger the formation of foam cells and fatty streaks along the vessel wall. These events lead to the development of atherosclerosis, where fatty deposits made of calcium, cholesterol particles, fibrin and other substances are deposited in the arteries.
However, this theory fails to answer some important questions related to heart disease:
- If cholesterol level is uniformly distributed across the length and breadth of the vascular system (arteries and veins), why does it majorly affect the coronary arteries of the heart and not the veins?
- Why don’t we get infractions in other organs and not just in the heart?
- Why don’t animals have heart attacks in the same frequency as humans?
Dr. Rath explains a new theory of cardiovascular disease, which suggests that long term deficiency of nutrients, especially vitamin C, impairs the structure and integrity of the arterial walls. And Lp (a) molecule (a type of cholesterol molecule) fills in to mend the damage and prevent the fatal blood loss that could happen if blood vessels continue to disintegrate in the absence of vitamin C.
So, what is the relation between low vitamin C levels and atherosclerosis?
Vitamin C deficiency and increase in Lp (a) levels
This concept was demonstrated in the 2015 study led by Dr. John Cha. It showed that low levels of vitamin C in the body results in an increase in Lp (a) levels. And accumulation of Lp (a) particles in the arterial wall causes atherosclerotic lesion development. [1]
The study also highlights another interesting relationship between vitamin C and Lp (a). It appears that we started to express the genes for Lp (a) molecule around the same time, around 40 million years ago, when we suffered a genetic mutation that took away the natural ability to make our own vitamin C. This relationship has great significance. It implies that humans started making Lp (a) molecule as a self-repair or self-defence mechanism that would save our life, by preventing scurvy and haemorrhagic blood loss in the absence of endogenous vitamin C.
This study is an extension of a concept published in 1990 by Dr. Matthias Rath together with two-time Nobel Prize winner Dr. Linus Pauling. They proposed that Lp (a) particle functions as a repair molecule and fills in for vitamin C to repair the damage within the vessel wall. The paper emphasized that Lp (a) is a “surrogate for ascorbate (is) suggested by the fact that this lipoprotein is found generally in the blood of primates and the guinea pig, which have lost the ability to synthesize ascorbate, but only rarely in the blood of other animals.” [2]
Vitamin C and collagen synthesis
Vitamin C is an important co-factor in collagen synthesis and repair. Collagen is a tough, fibrous protein present in the connective tissues found throughout the body, for example in skin, heart, digestive system, blood vessels, muscles, cartilage, tendons and ligaments. Collagen gives structure, strength and stability to the connective tissues.
When you don’t have enough vitamin C and other micronutrients in the body, this leads to poor and impaired collagen synthesis. Prolonged vitamin C deficiency causes scurvy. Since vitamin C is also required for other crucial biological processes like immune system functioning, wound healing, iron absorption and cholesterol metabolism, its chronic shortage in the body shows up as widespread symptoms – including weakness, poor wound healing, reduced appetite, bumps and bruising at hair follicles, aching muscles, anemia, swollen and bleeding gums, tooth decay, blurred vision, dry eyes, sensitivity to light, shortness of breath and chest pain. If left untreated, scurvy can even lead to internal bleeding, organ failure and death.
Heart Health
In terms of heart health, chronic vitamin C deficiency leads to breakdown of collagen and other connective tissue molecules in the artery wall. This kind of structural loss is first displayed in the blood vessel wall areas; for example, in the coronary arteries (arteries that supply blood to the heart muscle). It is because arteries are subjected to highest level of mechanical stress, owing to continuous beating of the heart. This kind of impairment in the arterial wall structure calls for urgent repair.
Interestingly, our body has a well-defined repair mechanism to deal with this damage. It sends Lp (a) particles to the arterial walls to initiate the repair process. However, this well-intentioned repair process soon goes erratic and results in the formation of plaque within the arteries. And it happens in the presence of persistent vitamin C deficiency.
How does it all work? What properties makes Lp (a) a fitting molecule to act as a surrogate for vitamin C? And most importantly, what exactly is Lp (a)?
Lp (a): Sticky cholesterol molecule that functions as a biological plaster
Your body needs fats to perform a wide range of functions that are absolutely critical for physical and mental well-being. But fats don’t mix well with water. They need some help to navigate through the bloodstream (which is mostly water) to reach various cells and tissues. This is where lipoprotein helps. Lipoproteins are small particles that function as vehicles to transport different types of fat molecules throughout the body.
Lipoproteins are made up of various type of fat molecules (such as triglycerides and cholesterol) surrounded by a layer of proteins and phospholipids. The protein in this structure is called apolipoprotein, serving many critical functions ranging from making lipoprotein soluble in blood, providing strong structure to lipoproteins and helping lipoproteins to bind to the receptors on the cells.
We are already familiar with high-density lipoprotein (HDL) and low-density lipoprotein (LDL). LDL particles contain a type of lipoprotein called apolipoprotein(b). And Lp(a) is a type of LDL particle that contains an additional protein on the surface called apolipoprotein(a) in addition to the usual apolipoprotein (b).
Apo (a) is a highly sticky protein, and this property gives Lp (a) particles a strong tendency to bind with various components of the connective tissue such as fibrin and collagen. They also easily bind to the cells of the endothelium. In addition, Lp (a) has many other properties:
- Lp (a) with its anti-fibrinolytic properties also promotes the formation of blood clots.
- Lp (a) particles due to their sticky nature are more firmly lodged in the arterial wall, where it gets attached to certain amino acids and initiates inflammatory responses.
Studies show that Lp (a) is one of the strongest genetic risk factors for all forms of cardiovascular disease (CVD), including heart attacks, stroke, coronary artery disease and peripheral vascular disease. However, the same binding and anti-fibrinolytic properties also help Lp (a) to speed up the wound healing process and launch other repair mechanisms within cells, properties that it shares with vitamin C.
How does Lp (a) compensate for vitamin C deficiency?
Shortage of vitamin C in the body leads to impaired collagen synthesis and repair, a process that weakens and damages the connective tissue in the arteries. This causes loss of structure and integrity in the vascular walls and may lead to fatal haemorrhagic blood loss.
Now, the liver produces Lp (a), which works as a mobile repair molecule to compensate for this structural damage. Lp (a) essentially fulfils two very important functions:
- Lp (a) uses LDL as a carrier to reach the damaged site, in this case the arteries. LDL provides cholesterol and other fats to make new, healthy cells. (Contrary to popular belief, cholesterol is not your enemy. It has many critical functions in the body. For example, you need cholesterol to make steroid hormones, vitamin D and bile acids to digest fats. Your cell membranes and myelin sheath around the nerve cells are made of cholesterol. In addition, the liver sends LDL cholesterol molecule to the site of injury to repair damaged cells. You also need cholesterol to produce healthy, new cells).
- The sticky apo (a) protein in Lp (a) particle binds to the arterial wall to compensate for the faulty collagen and to prevent blood vessels from falling apart and bleeding.
While it starts as a repair process to counter a lack of vitamin C and to preserve the integrity of vascular walls, the entire process, if it lasts long-term, leads to plaque deposition within the arterial walls. [3]
Humans, and some animals like guinea pigs and bats, have lost their ability to produce their own vitamin C. Most other animals, however, naturally produce enough vitamin C. This protects their arteries from structural damage and the resulting atherosclerosis. This also answers why animals rarely (extremely rarely) die of heart attacks.
Summary of findings from the 2015 study on cardiovascular disease
- Chronic vitamin C deficiency increases Lp(a) levels in the blood.
- Accumulation of Lp(a) in the arterial walls results in the onset and progress of atherosclerosis.
- Increased levels of Lp(a) in the blood is not the main underlying cause of cardiovascular disease. It is rather an indication that connective tissue of the blood vessels is falling apart, and the body has initiated a much needed, life-saving repair process by calling upon Lp (a) particles and other fat molecules at the site of damage.
- Usually, a diet high in fats is believed to cause atherosclerosis. However, vitamin C deficiency serves as an independent risk factor for the development of atherosclerosis.
References:
- Cha et al. Hypoascorbemia induces atherosclerosis and vascular deposition of lipoprotein(a) in transgenic mice. Am J Cardiovasc Dis. 2015
- Rath M, Pauling L. Hypothesis: lipoprotein(a) is a surrogate for ascorbate. Proc Natl Acad Sci U S A. 1990
- Breakthrough towards the natural control of cardiovascular disease, Dr. Matthias Rath, 22-4-2015. YouTube. (Video)
