| CleanDNA News |
Of Mice, Guinea Pigs and MenIn 1941, an Ottawa pathologist named J.C. Paterson first hypothesized that the fragility of capillaries in atherosclerotic plaques might be related to vitamin C deficiency. Animal studies supported his ideas, including those in the guinea pig, one of the few animals (like humans) that are unable to synthesize their own vitamin C. Guinea pigs are herbivores, and have poor control mechanisms for cholesterol. In fact, high consumption of cholesterol in the guinea pig leads to deposition of cholesterol throughout the body. In the 1950s, G.C. Willis studied the issue by feeding guinea pigs a high cholesterol diet along with varying levels of vitamin C. Vitamin C supplementation reduced the severity of plaque formation in all animals, and injected vitamin C prevented plaque formation in about half the animals. Also, scientists working with a strain of laboratory mouse having a mutation in gulonolactone oxidase have found that it suffers damage to the aorta if not supplemented with vitamin C. This is the missing vitamin C biosynthetic enzyme in humans which confers our absolute need for dietary intake of the vitamin. Questions have thus arisen about the lack of well-designed human studies, which the early researchers assumed would follow in logical order. As stated by Hickey and Roberts, "almost all the thousands of medical papers published in this area (human studies) have used doses too small to be effective... the delay is unfortunate... if the hypothesis is correct... people continue to die unnecessarily."
From Ascorbate: The Science of Vitamin C |