The natural history of ascorbic acid in the evolution of the mammals and primates and its significance for present day man

TitelThe natural history of ascorbic acid in the evolution of the mammals and primates and its significance for present day man
Jahr der Veröffentlichung1972
AutorenStone, I.
Seitenanzahl82 - 89

Die Meisten Tierarten können Vitamin C selbst produzieren. Es ist eine alter Erungenschaft in der Evolution. Nur einige Ausnahmen unter den Tieren, darunter der Mensch haben einen Gendefekt fixiert, der die Biosynthese des Vitamin C verhindert. Diese sind dann auf die externe Zufuhr angewiesen.

Evidence is presented that the enzyme systems for the important synthesis of ascorbic acid are of very ancient origin, beginning long before the plant and animal lines diverged. The progressive vertebrate evolution of these enzymes are traced through the fish, 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, which destroyed this animal's ability to produce ascorbic acid from blood glucose. The progeny of this mutated animal developed into the present day members of the primate suborder, Anthropoidea. The non mutated primates were the ancestors of the present suborder, Prosimii. Extrapolation of this data into the primate fossil record indicates the mutation to have occurred in the period between the late Cretaceous and late Paleocene and may have been caused by the same nearby supernovae 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, still carry this defective gene and during prehistoric and historical times it has been responsible for more deaths and more sickness than any other single factor. The vital importance of ascorbic acid in many phases of human physiology has been underrated for the past 60 yr. Ascorbic acid is a liver metabolite produced in nearly all mammals in large daily amounts. Because of this defective gene, Man is suffering from a mammalian genetic liver enzyme disease, a true 'inborn error of carbohydrate metabolism' named Hypoascorbemia. Scurvy is not a distinct disease entity but merely the final fatal sequelae of uncorrected Hypoascorbemia. This genetic approach provides the rationale for the use of large daily doses of ascorbic acid.

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