Some knowledge regarding vitamin deficiencies is derived from human depletion and repletion studies. Subjects are fed a balanced diet which is carefully controlled to be deficient in the vitamin of choice. The researchers then assess the physiological changes in order to understand the functions of the vitamin. These functions can be verified on re-introduction of the nutrient to the diet during repletion. Similar studies can be performed with animals, but depletion can be more severe. In recent decades human depletion studies have began to investigate a new type of vitamin status called the vitamin insufficiency. Vitamin insufficiencies do not produce classical deficiency symptoms because the diet contains a small amount of the nutrient. Instead sub-clinical changes that can alter nuances in metabolic pathways and physiological function are caused by a low and inadequate intake, usually over a large proportion of the life of the individual.
Vitamin K is required for the correct clotting of blood as it forms γ-carboxyglutamyl residues in the vitamin K dependent clotting factors (VII, IX and X). Vitamin K insufficiency is therefore though to cause alteration in the ability of blood to clot. Researchers1 have tested this hypothesis by feeding 10 adult male subjects a vitamin K restricted diet for 40 days. Intakes of phylloquinone (plant based vitamin K) fell from 82 µg per day to below 40 µg per day during the study. This was reflected in a mean plasma level of phylloquinone that fell from 0.87 to 0.46 ng/mL. When the subjects took 50 µg per day of phylloquinone in a tablet, plasma levels rose to 0.56 ng/mL and when they took 500 µg per day levels rose to 1.66 ng/mL. The vitamin K restricted diet was accompanied by deleterious changes to a clotting assay, which was reversed upon supplementation with vitamin K.
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