Vitamin C – Missing in Action! 

   Possibly the most important discovery of Dr. Linus Pauling, the 2-time winner of the Nobel Prize, was discovering the critical link between vitamin C and arterial disease.  Vitamin C, along with the amino acids proline and lysine, are the essential nutrients responsible for healthy arteries. 

   The curiosity about vitamin C started when we became aware of the huge difference between humans and most other animals in the production of vitamin C.  Humans do not produce vitamin C in our bodies, while other mammals of similar usually produce from 8,000 – 15,000 mg of vitamin C!  Why such a difference – and why is our ‘supposed’ requirement only 60+ mg?  That is a huge difference in animals supposedly similar. 

    Evidence for when our enzyme systems began to differ for the important synthesis of ascorbic acid (vit. C) are very ancient.  The progressive vertebrate evolution of these enzymes has been traced through the fishes, amphibians, reptiles, birds and mammals.   

   Shortly after the appearance of the primates, a genetic mutation occurred on the gene for the liver enzyme L-gulonolactone oxidase.  This destroyed our ability to produce ascorbic acid from blood glucose.  (Interestedly, primate fossil records indicate the mutation to have occurred in the period the same explosion which was possibly responsible for the extinction of the dinosaurs and the disappearance of many invertebrates in the late Cretaceous.) 

   Members of the genus Homo (present day Human) still carry this defective gene.  During prehistoric and historical times it has been responsible for more deaths, more sickness and human misery and more changes in history, than any other single factor.  Now we call this missing ascorbic acid a “vitamin” and are becoming aware of its importance.  Because of this defective gene, mankind is suffering from a mammalian genetic liver-enzyme disease.  We call one of its expressions, “Scurvy”.  We call another expression, “Arterial Disease”!  

Collagen Holds Everything Together 

   Collagen is the protein that forms connective fibers in tissues such as skin, ligaments, cartilage – and artery linings!  Collagen fibers keep bones and blood vessels strong, and help to anchor our teeth to our gums.  Collagen is also required for the repair of blood vessels, bruises, and broken bones.  As the most abundant protein in the body, collagen accounts for more mass than all the other proteins put together! 

   As we said, vitamin C, along with the amino acids proline and lysine, is essential for the formation of healthy collagen.  Some other vitamins and minerals act as catalysts but vitamin C is the ‘star’ as it combines with lysine and proline to form pro-collagen.  Pro-collagen is then used to manufacture several types of collagen found in different tissues throughout the body. 

   Without vitamin C, collagen formation is disrupted, resulting in a wide variety of problems throughout the body.  Scurvy, the disease caused by vitamin C deficiency, is really the disruption of the body’s ability to manufacture collagen and connective tissues.  With scurvy, the body literally falls apart as collagen is broken down and not replaced.  The joints begin to wear down as tendons shrivel and weaken.  The blood vessels begin to fall apart, leading to bruising and bleeding as vessels rupture (hemorrhage) throughout the body.  Teeth loosen and fall out as the gums and the connective tissues holding teeth also begin to erode.  Organs, once held firmly together by connective tissues, also lose structural strength and begin to fail.  In time, the various body tissues weaken and the immune system and heart give out, leading to death. 

Dissolving Plaque 

   Another quality about vitamin C is that increased levels cause atherosclerotic plaque deposits to dissolve!  Some studies have shown plaque deposits in patients who receive large amounts of vitamin C to have decreased as much as 30%!  Studies indicate that vitamin C is involved in helping the chelation of the calcium ions in the plaque deposits.  Thus, it complements EDTA, garlic and lecithin - which is helping dissolve the cholesterol aspect of plaque. 

   Dr. Willis conducted a study at Queen Mary Veterans' and St. Anne's Hospitals.  He took two groups, one group received no treatment and the other was given 1500 mg of vitamin C per day.  After a year, the atherosclerotic plaque deposits in the control group either stayed the same or grew larger.  The plaque deposits in the patients who were getting the Vitamin C actually decreased in 30% of the cases. This was the first time in history that any treatment had demonstrated a reversal in the growth of atherosclerotic plaque deposits in human beings! 

   Dr. Pauling then announced, in 1989, a breakthrough in how we view and treat heart disease.  Pauling announced that the deposits of plaque seen in atherosclerosis were not the cause of heart disease.  They were the result of our bodies trying to repair the damage caused by long-term vitamin C deficiency.  If the body can’t use collagen, it will use sticky cholesterol (causing pIaque) rather than die.  In essence, Pauling believed that heart disease is a form of scurvy, and plaque is the body’s attempt to reinforce and patch weakened blood vessels and arteries that would otherwise rupture.  Pauling showed that heart disease can be prevented or treated by taking vitamin C and other supplements. 

   To help remove existing plaque while strengthening weak and damaged arteries, Pauling recommended a combination of vitamin C and the amino acids lysine and proline.  As mentioned previously, the body produces collagen from lysine and proline. Pauling reasoned that by increasing concentrations of lysine and proline in the blood, Lp(a) molecules would bind with the free lysine, rather than with the lysine strands exposed by the cracks in blood vessels.

   Pauling discovered that plaque deposits found in human aortas are made up of a special form of cholesterol called lipoprotein (a) or Lp(a), not from ordinary LDL cholesterol.  Lp(a) is a special form of LDL cholesterol that forms the thick sheets of plaque that obstruct arteries. 

   Another finding was that plaque deposits are not formed randomly throughout the circulatory system. This was first reported in the early 1950s when a Canadian doctor, G. C. Willis, MD.  He observed that plaque always forms nearest the heart, where blood vessels and arteries are constantly being stretched and bent, rather than being spread evenly throughout the entire cardiovascular system.  Willis also noted that plaque deposits always occur in regions that are exposed to the highest blood pressures, such as the aorta, where blood is forcefully ejected from the heart. 

   In 1985, a team of researchers verified that plaque only forms in areas of the artery that become damaged.  Just as cracks form in a garden hose that has become weak and worn from constant bending and high-pressure, cracks form in the lining of the arterial wall.  As these tiny cracks open up they expose strands of the amino acid lysine (one of the primary components of collagen) to the blood stream.  It is these strands that initially attract Lp(a) - an especially sticky form of cholesterol that is attracted to lysine. 

   Drawn to the break, Lp(a) begins to collect and attach to the exposed strands.  As Lp(a) covers the lysine strands, free lysine in the blood is drawn to the growing deposit.  Over time, this process continues as lysine and Lp(a) are both drawn from the blood to build ever-larger deposits of plaque. This process gradually forms plaque and reduces the inner diameter of the vessels. 

Heart Disease is a Result of Emergency Response to Scurvy 

   Pauling recognized a similarity to underlying processes seen in scurvy.  He also saw similarities between human and animal atherosclerosis that pointed to a connection with scurvy.   

• First, cardiovascular disease does not occur in any of the animals that are able to manufacture their own vitamin C!  (Many animals produce large amounts of vitamin C that are equivalent to human doses ranging from ten to twenty grams per day.) 
• Second, the only animals that produce Lp(a) are those which, like man, have also lost the ability to produce their own vitamin C, such as apes and guinea pigs.  
• Putting all the pieces of the puzzle together, Pauling suggested that the ability to form plaque is really the body’s attempt to repair damage caused by a long-term deficiency of vitamin C. 

   He knew that our ancestors lived in tropical regions where the diet consisted primarily of fruits and vegetables. With a daily intake estimated to be in the range of several hundred milligrams to several grams per day, our ancestors easily survived without the gene required to manufacture vitamin C.  Almost unnoticed, this mutation was passed on to successive generations, and only became a problem when early humans began to spread to other regions of the world.  In effect, when humankind left the garden, the lack of a reliable and adequate supply of dietary vitamin C led to scurvy. 

   Pauling thought that scurvy was one of the greatest threats to humankind’s early survival, and believed that the loss of blood during times of vitamin C deficiency, particularly during the Ice Ages, likely brought humans close to the point of extinction. 

Plaque is a Life Saver! 

   The core of Pauling’s work is that, over time, the body developed a repair mechanism that allowed it to cope with the damage caused by chronic vitamin C deficiency.  The repair mechanism is as elegant as it is simple.  When arteries became weak and began to rupture, the body responded by gluing the damaged areas together with Lp(a) to prevent a slow death from internal bleeding. 

   In essence, plaque is the body’s attempt to patch blood vessels damaged by low-level scurvy.  Accordingly, Pauling believed that conventional triggers of plaque formation, such as free radicals, homocysteine and oxidized cholesterol, are actually just additional symptoms of scurvy.  They use the breach in the arterial lining as an opportunity to attack vulnerable parts. 

   Pauling’s theory was unique in that it addressed a fact never explained by older, mainstream theories.  Specifically, Pauling finally explained why plaque isn’t randomly distributed throughout the body, but restricted to areas of high mechanical stress.  A surprising number of animal studies have been found to support Pauling’s theory.  

   Research conducted with animals that cannot make their own vitamin C found that when vitamin C levels are reduced, collagen production drops and blood vessels become thinner and weaker.  Additional studies also confirm that when animals are deprived of vitamin C, their bodies respond by increasing blood levels of Lp(a) and forming plaque deposits to strengthen arteries and prevent vessel ruptures. 

References: 

Boonmark NW; Lou XJ; Yang ZJ; Schwartz K; Zhang JL; Rubin EM; Lawn RM. Modification of apolipoprotein(a) lysine binding site reduces atherosclerosis in transgenic mice. J Clin Invest 1997 Aug 1. 

Carr AC, Frei B. Toward a new recommended dietary allowance for vitamin C based on antioxidant and health effects in humans. American Journal of Clinical Nutrition 1999. 

Gladys Block, "Vitamin C and Cancer Prevention: The Epidemiologic Evidence," American Journal of Clinical Nutrition; 1991; 53:270S-82S. 

Jacques PF, Chylack LT, Jr., Hankinson SE, et al. Long-term nutrient intake and early age-related nuclear lens opacities. Arch Ophthalmol. 2001;119(7):1009-1019. 

Marcoux C; Lussier-Cacan S; Davignon J; Cohn JS. Association of Lp(a) rather than integrally-bound apo(a) with triglyceride-rich lipoproteins of human subjects. Biochim Biophys Acta 1997 Jun 23;1346(3). 

McCully KS, Homocysteine metabolism in scurvy, growth and arteriosclerosis. Nature 1971. 

Pauling L, Rath M. Pro. Nat. Acad. Sci USA, Vol 87, pp 9388-9390, Dec 1990. 

Simon JA, Hudes ES. Serum ascorbic acid and gallbladder disease prevalence among US adults: the Third National Health and Nutrition Examination Survey (NHANES III). Arch Intern Med. 2000. 

S.K. Gaby and V.N. Singh, "Vitamin C," – Vitamin Intake and Health: A Scientific Review, S.K. Gaby, A. Bendich, V. Singh and L. Machlin (eds.) Marcel Dekker, N.Y. 1991. 

Stephen R, Utecht T. Scurvy identified in the emergency department: a case report. Journal of Emerg Med. 2001. 

Stubbs P; Seed M; Moseley D; O’Connor B; Collinson P; Noble M. A prospective study of the role of lipoprotein(a) in the pathogenesis of unstable angina. Eur Heart J 1997 Apr;18(4).