Vitamin C the scorbutic diet was fed. Men in both studies on a diet devoid, or nearly devoid, of vitamin C had blood levels of vitamin C too low to be accurately measured when they developed signs of scurvy and, in the Iowa study, at this time were estimated (by labeled vitamin C dilution) to have a body pool of less than 300 mg, with daily turnover of only 2.5 mg/day, implying an instantaneous half-life of 83 days by this time (elimination constant of 4 months). Vitamin C has a definitive role in treating scurvy, which is a disease caused by vitamin
Vitamin A deficiency reference point for the extent of deficiency (with mortality increasing with severity of the eye disease). In a longitudinal study of preschool Indonesian children, susceptibility to disease increased nine times when severe VAD was present. The reason for the increased infection rate in vitamin A deficient populations is the T-killer cells require retinoids to proliferate correctly. Retinoic acid binds the promoter region of specific genes, so activates the transcription process and cell replication. A vitamin A-deficient diet will have a very limited surplus of retinol, so cell proliferation and replication will be suppressed, contributing to a reduced number of T-cells