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The possibility that sustained folic acid intake would deplete vitamin B-12 independent of hematopoiesis suggests a plausible alternative mechanism based on the known details of the renal handling of holoTC, whereby folic acid might interfere with holoTC reuptake or cause its sequestration in the kidney, promoting the excretion of holoTC and further depleting metabolically active vitamin B-12 during vitamin B-12 deficiency

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