The Vitamin C and Heart Disease Connection
Recent statistics released by the Center for Disease Control and Prevention revealed that heart disease is still the leading cause of death in the U.S. with just shy of 600,000 deaths reported in the year 2011. Thankfully, researchers have discovered many variables which contribute to the development of different forms of heart disease and cardiovascular diseases, and medicines that can save lives in emergency medical situations. Yet, efforts are being directed towards creating a drug designed to alleviate symptoms in non-emergency medical situations, while very little focus on addressing the actual lifestyle, causative factors that lead to the development and continued existence of the disease. The emerging understanding of a compound measured in the blood seems to be a much more accurate marker in predicting a persons risk in developing certain forms of cardiovascular disease (CVD), but also offers valuable information on how a person can improve their health. Through providing the body with optimal levels of certain nutrients whether through diet alone or diet together with supplementation may decrease the risk of developing certain forms of CVD .
In 1994, two doctors obtained a patent for their extensive research within various forms of cardiovascular disease; such as atherosclerosis, arteriosclerosis and coronary artery disease in connection with the amount of vitamin C intake and the presence of a molecule in the blood known as Lp(a). Linus Pauling, known to many as the founder of modern chemistry, the only person to win two unshared Nobel Prizes and who holds 48 honorary Ph.D.’s, alongside with his colleague Matthias Rath, M.D., obtained a patent for what is now known as: The Unified Theory of Human Cardiovascular Disease. It consist of a thorough theoretical explanation of what they have found through their years of research within biochemistry and biology. It explains how humans, being one of the few species of animals who lack the ability to produce Vitamin C from glucose, need to obtain optimal levels of vitamin C in their diet or through supplementation, otherwise face an increased likelihood of elevated blood levels of the Lp(a) particle. These particles acts as a substitute for vitamin C in repairing damage that has occurred to vascular walls. Unfortunately this molecule doesn’t quite repair the walls in the same way which Vitamin C can. Instead of repairing and rebuilding damaged collagen and elastin protein strands and restoring the vascular wall back to its original form, Lp(a) seems promote the formation and growth of blood clots (thrombogenesis) while also inhibiting the enzymatic breakdown of a protein present in pre-existent clots (fibrinolysis). Lp(a) also increases the release of inflammatory compounds which further lead to the thickening and proliferation of the smooth muscle cells that line the vascular wall. The actions that Lp(a) can elicit are viewed as a triple-threat by some cardiologists since over time this can increase the risk of developing the aforementioned Cardiovascular Diseases (CVD’s). Although the presence of Lp(a) may have once helped a population survive in an environment or through an era such as an ice-age, where they were deprived from or restricted of a diet rich in optimal amounts of Vitamin C. When one actually looks at the long term health effects it certainly seems to be healthier to have the body’s vascular walls protected and repaired from the presence of Vitamin C rather than Lp(a).
Since Pauling and Rath had presented their theory, there has been a lot more research carried out and discoveries made on the effects of Lp(a), and it’s connection with CVD. Researchers have discovered that there are many different sizes of the apoprotein (a) molecule, which is part of the overall Lp(a) particle. This is of great significance because some sizes have not been found to be associated with an increased risk of heart disease, while other sizes, particularly the smaller size version of the apoprotein a molecule, are strongly associated with a greater risk for the development of atherosclerosis. A person’s genetics determines the size. What determines the quantity present in the blood is another question that researchers are still discovering. However, it is very likely Pauling and Rath’s theoretical explanation was somewhat accurate in that lifestyle factors that influence the amount of vitamin C present in the body and the amount of inflammation and damage done to vascular walls on a day by day basis can have a strong influence and correlation with the amount of Lp(a) produced by the liver and released into the bloodstream.
If Pauling and Raths patented theory is accurate then it’s very possible that one of the best steps one could take is to provide the body with optimal levels of the appropriate nutrients needed to build, repair and maintain healthy vascular walls while also reducing the extent of damage inflicted upon the vascular walls as a result of exposure to substances such as free radicals, homocysteine or autoimmune reactions linked to food allergies and leaky gut syndrome. Healthy lifestyle habits such as following a diet high in whole foods, and fresh, organic fruits and vegetables while low in processed foods, refined sugars, hydrogenated fats and trans-fatty acids can help significantly. Limiting your exposure to smoke, whether first or second hand smoke can also have a strong influence.

Resources:
Segala, M. & Needham, A. (2003) Life Extentions Foundation’s Disease Prevention and Treatment – Expanded Fourth Edition (pp. 466-467) Hollywood, Florida: Life Extention Media
Holford, P., (1999) The Optimum Nutrition Bible, (pp.117-121) Crossing Press Inc., Freedom CA
http://www.cdc.gov/nchs/fastats/lcod.htm
http://orthomolecular.org/library/jom/1992/pdf/1992-v07n01-p005.pdf
http://supervitaminec.com/documents/US5278189-Linus-Pauling-Matthias-Rath-megadoses-vitamine-c.pdf
http://www.webmd.com/heart-disease/news/20090609/lipoprotein-a-linked-to-heart-attacks
http://www.hindawi.com/journals/chol/2010/306147/
http://www.mayoclinic.com/health/niacin/NS_patient-niacin/DSECTION=evidence
http://en.wikipedia.org/wiki/Lipoprotein(a)
