Scurvy fever, convulsions, and eventual death are frequently seen. Scurvy, including subclinical scurvy, is caused by a deficiency of dietary vitamin C since humans are unable to metabolically make this chemical. Provided diet contains sufficient vitamin C, the lack of working GULO enzyme has no significance, and in modern Western societies, scurvy is rarely present in adults, although infants and elderly people are affected. Virtually all commercially available baby formulas contain added vitamin C, preventing infantile scurvy. Human breast milk contains sufficient vitamin C, if the mother has an adequate intake. Commercial milk is pasteurized, a heating process that destroys the
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