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Supplementation improves survival in mouse model of human vitamin C deficiency

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Reprinted with the kind permission of Life Extension.

March 9 2016. Research reported on February 20, 2016 in Aging found that supplementation with vitamin C (ascorbate) corrects some of the deficits observed in mice bred to lack an enzyme that rendered them, like humans, unable to manufacture the vitamin.

“Most mammals are capable of synthesizing their own ascorbate and are thus not prone to develop vitamin C deficiency,” authors Lucie Aumailley and colleagues explain. “Humans, however, have a mutation in the gene encoding the enzyme gulonolactone oxidase (GULO) necessary for the last step of ascorbic acid synthesis.”

After weaning, the animals were supplemented with a low dose, high dose or no vitamin C, and serum metabolites and other factors were measured at four months of age. Those that were not supplemented with the vitamin were euthanized within six weeks due to poor health and significant weight loss. While mice that received the low dose of vitamin C survived longer than unsupplemented mice, they also experienced poor health and weight loss over up to 16 months that necessitated eventual euthanasia. However, animals that received the high dose experienced a median life span of 23 months and a maximum life span of 32 months, while the median achieved in non-modified untreated animals was 23.8 and the maximum was 30 months. Supplementation with vitamin C was additionally associated with improved levels of several lipids and cardiovascular risk factors.

“Median life span of the different cohorts of mice (including untreated wild type mice) correlated positively with the mean levels of ascorbate measured in the serum of each group of mice,” the authors note.

“Our study demonstrates the impact of suboptimal levels of ascorbate on longevity and the metabolic profile of a mouse model, that similar to humans, lacks the enzyme required for the synthesis of ascorbate,” they conclude.

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