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Vitamin C Deficiency and Scurvy Are Not Only a Dietary Problem but Are Codetermined by the Haptoglobin Polymorphism

¹ Department of Clinical Chemistry, University Hospital Ghent, Ghent, Belgium
² Department of Cardiology, University Hospital Ghent, Ghent, Belgium
³ Department Languages and Cultures, of South and East Asia, Ghent University, Ghent, Belgium

^aAddress correspondence to this author at: Department of Clinical Chemistry, University Hospital Ghent, De Pintelaan 185 (2P8), B-9000 Ghent, Belgium. Fax 32-9-240-4985; e-mail joris.delanghe{at}ugent.be.

Ascorbic acid (vitamin C) is prone to oxidation in vivo. The human plasma protein haptoglobin (Hp) shows a genetic polymorphism with 3 major phenotypes (Hp 1-1, Hp 2-1, and Hp 2-2) that show important functional differences. Despite an adequate nutritional supply, in Hp 2-2 individuals (most common among Asian populations) vitamin C is markedly lower in concentration and particularly prone to oxidation in vivo. Therefore, susceptibility to subclinical and clinical vitamin C deficiency (scurvy) is partly genetically determined. The genetic advantage of the Hp1 allele as a vitamin C stabilizing factor helps to elucidate the direction and successes of long-distance sea crossing human migrations in history. Clinical trials demonstrated Hp phenotype–related effects of antioxidant treatment. Because vitamin C is a first line antioxidant, Hp polymorphism and its effects on vitamin C have major clinical consequences; a marked difference in genetic susceptibility toward atherosclerosis between Hp phenotypes is attributable to variation in LDL oxidation. The classical view of vitamin C and scurvy being a pure nutritional condition needs to be updated. These findings should foster research investigating the role of Hp polymorphism in human disease, and in vitamin C deficiency and atherosclerosis in particular.