Scurvy is a disease resulting from a deficiency of vitamin C. Humans and certain other animal species require vitamin C in their diets for the synthesis of collagen. In infants, scurvy is sometimes referred to as Barlow's disease, named after Sir Thomas Barlow,[1] a British physician who described it in 1883.[2] However, Barlow's disease may also refer to mitral valve prolapse. Other eponyms for scurvy include Moeller's disease and Cheadle's disease. The chemical name for vitamin C, ascorbic acid, is derived from the Latin name of scurvy, scorbutus, which also provides the adjective scorbutic ("of, characterized by or having to do with scurvy").
A child presenting with a "scorbutic tongue" due to what proved to be a vitamin C deficiency.
Scorbutic gums
Typical symptoms of scurvy are initially fatigue, followed by formation of spots on the skin, spongy gums, and bleeding from the mucous membranes. Spots are most abundant on the thighs and legs, and a person may look pale, feel depressed, and be partially immobilized. As scurvy advances, there can be open, suppurating wounds, loss of teeth, yellow skin, fever, neuropathy and finally death from bleeding.[3]
Treatment is by a vitamin C-rich diet, whereby complete recovery from incipient scurvy takes less than two weeks. Vitamin C is widespread in plant tissues, with particularly high concentrations occurring in capsicum fruit (especially sweet green peppers), cruciferous vegetables (such as kale, broccoli and brussels sprouts), and citrus fruits (especially oranges). Organ meats such as liver contain more vitamin C than muscle meat. Cooking significantly reduces the concentration of vitamin C as does exposure to air, copper, iron, and other transition metal salts.
Scurvy does not occur in most animals as they can synthesize their own vitamin C. However, humans and other higher primates, guinea pigs, most or all bats, and some species of birds and fish lack an enzyme necessary for such synthesis and must obtain vitamin C through their diets.
Historically, Hippocrates (c. 460 BCE–c. 380 BCE) described scurvy, and herbal cures for scurvy have been known in many native cultures since prehistory. Nevertheless, treatment was inconsistent, and scurvy was one of the limiting factors of marine travel, often killing large numbers of the passengers and crew on long-distance voyages.[4] While there is earlier evidence (from the voyages of Vasco da Gama and James Lancaster, for example) that citrus fruit had a curative effect on scurvy, it was a Scottish surgeon in the Royal Navy, James Lind, who first proved it could be treated with citrus fruit in experiments he described in his 1753 book A Treatise of the Scurvy.[5] These experiments in fact represented the world's first clinical trial. Unfortunately no prominence was given to this finding in a book which was long and contradictory. Lind's findings did not conform to the theories of his time, that scurvy was the result of poor digestion and the consumption of preserved meat and moldy water, and as a result had little impact on medical thinking. It would be 40 years before practical seamen and surgeons insisted on issuing lemon juice and effective prevention became widespread.[6] Scurvy remained a problem during expeditions and in wartime until the mid-20th century.