History of Scurvy

Scurvy


Scurvy is a disease caused by lack of vitamin C in the body. The word scurvy is dated to the sailors and the pirates on the long sea voyages but the "land scurvy" greatly affected numerous Crusaders from Europe who spent many months traversing through the Mild East. A re-known physician from Scott James Lind, in 1747, found that the lemons and the oranges could cure the disease but unfortunately the sailors did not benefit from the therapy. The disease was documented by the Hippocrates in the 13th century and by 1550BC, the Egyptians had recorded the symptoms associated with the disease.


The Rediscovery


The knowledge that ingesting the food rich in vitamin C can cure the disease has been rediscovered in the early 20th century. In 1497, expedition of the Vasco da Gama, shows that the citrus fruits could cure it and that was confirmed by the Cabral Alvares Pedro and associated crews in 1507. Moreover, the Portuguese planted vegetables and the fruits in Halena Saint, the stopping point for the voyages from Asian countries (Eddy et al, 1929). The sick suffering from scurvy were left at the same point to be taken home and if recovered, by the next ship. Major treatment to eradicate the infection since the 13th century has almost eliminated the disease in most parts of the world with the disease burden left on the developing countries where instances of malnutrition is still very common.


Causes of scurvy


The disease is caused by lack of vitamin C or ascorbic acid in the body. In the modern developed nations, the disease rarely occurs in adult age groups although it is more common in elderly and the infants who are mostly affected by the disease. However, the commercially available infant formula has the Vitamin C added in its components to prevent the development of the infantile scurvy. With adequate intake of diet rich in Vitamin C, the human breast milk can produce sufficient amount of Vitamin C needed by the infant. The heating process that occurs with commercial milk pasteurization results in the destruction of the vitamin leading to its deficiency among infants consuming the products. The disease is significantly associated with malnutrition and micronutrient deficiencies such as pellagra and beriberi (Mussini et al, 1967). The association with malnutrition explains its high prevalence in the developing countries that depend on the external food aids from other nations. In the industrialized nations, although rare, the disease is associated with poor dietary choices among the citizens who choose to prefer other types of meals that may be insufficient in the amount of the ascorbic acid.


Pathogenesis and effect on bones


Ascorbic acid is crucial in many biosynthetic pathways by facilitating the amidation and hydroxylation reactions. It acts as the cofactor in the synthesis of collagen by forming the component of lysyl hydroxylase and prolyl hydroxylase. The two enzymes facilitate the hydroxylation of the lysine and proline amino acids in the collagen (Williams et al, 1967). Moreover, the hydroxy lysine and hydroxy proline stabilize the collagen through crosslinking the peptides within the collagen. When collagen fibrillogenesis is defective, it impairs the process of wound healing. Moreover, collagen is an integral component of the bone hence defects in collagen synthesis results in poor bone formation, a characteristic feature observed in individuals suffering from lack of vitamin C. Again, the capillaries are very fragile due to defective connective tissue that results to increased propensity to bleeding with minimal trauma. Untreated scurvy is invariably fatal.


Effect on Bones


Vitamin C deficiency results in the alterations of structural collagen in the bones. The inadequacy results to defect in the formation of the osteoid matrix and increases the levels of bone resorption. The increased bone resorption makes them to be very weak and unable to bear weight, stress and strains imposed on them (Ortner, 1997). Images from the bones taken due to lack of vitamin C shows loss of the joint spaces, osteolysis, osteopenia, osteonecrosis and proliferation of the periosteal. Moreover, cortical osteoporosis and trabecular necrosis are very common with the disease. The subperiosteal bleeding causes severe lower limb pain in children. The laboratory tests show non-specific abnormalities include low levels of albumin, cholesterol and anemia. The finding of the serum ascorbic acid less than 2.5 mg/l confirms the diagnosis of scurvy and requires prompt supplementation of vitamin C to cure the symptoms.


How it became prominent


The development and research on scurvy has progressed over centuries since the 13th century when the sailors were affected with the disease and did not have the means of treating the disease. Major advancement in establishment of causative agent warranted thorough research that resulted in association of scurvy with lack of vitamin C in the body. The disease has become highly prominent in the third world countries due to its association with malnutrition that hits hard the countries which depend on foreign aids for food security (Crandon et al, 1940). The industrialized nations register a low prevalence of the disease due to its eradication by fortification of the food and better strategies in preventing malnutrition among the poor people in the country.


Treatment


Treatment of scurvy involves the administration of vitamin C supplement either by injection or oral route. The recommended dosages are as follows;


- One to two grams per day for two to three days


- Five hundred milligram for the next seven days


- One hundred milligram for about one to three months. Within 24 hours, patients can expect to see an improvement in fatigue, lethargy, pain, anorexia, and confusion. Bruising, bleeding, and weakness start to resolve within 1 to 2 weeks.


Prevention


The disease is easily preventable by taking a diet that is rich in vitamin C such as bell peppers, broccoli, sweet peppers, guava, blackcurrants, parsley, chili peppers, and kiwifruit. Other notable food rich in vitamin C includes oranges, lemons, strawberry, and papaya. Vegetables are also rich sources of vitamin C and they include spinach, cabbage, potatoes, and brussels sprouts (Lind, 1772). Although there is redundancy in the presence of a well-balanced diet, some nutritional supplements provide excess vitamin C than the required amount for the prevention of scurvy. The animal products such as oysters, liver, whale skin, brain, adrenal medulla, and the spinal cord are rich sources of ascorbic acid and are useful in the treatment of scurvy. Prevention can also be done by administration of vitamin C as follows;


- Up to 6 months: 40 mg, as normally supplied though breastfeeding


- 7 to 12 months: 50 mg


- 1 to 3 years: 15 mg


- 4 to 8 years: 25 mg


- 9 to 13 years: 45 mg


- 14 to 18 years: 75 mg for men and 65 mg for women


- 19 years and above: 90 mg for men, 75 mg for women

Bibliography


Lind, James. A Treatise on the Scurvy. S. Crowder, 1772.


Crandon, John H., Charles C. Lund, and David B. Dill. "Experimental human scurvy." New England Journal of Medicine 223, no. 10 (1940): 353-369.


Ortner, Donald J., and Mary Frances Ericksen. "Bone changes in the human skull probably resulting from scurvy in infancy and childhood." International Journal of Osteoarchaeology 7, no. 3 (1997): 212-220.


Ortner, Donald J., Erin H. Kimmerle, and Melanie Diez. "Probable evidence of scurvy in subadults from archeological sites in Peru." American Journal of Physical Anthropology 108, no. 3 (1999): 321-331.


Peterkofsky, Beverly. "Ascorbate requirement for hydroxylation and secretion of procollagen: relationship to inhibition of collagen synthesis in scurvy." The American journal of clinical nutrition 54, no. 6 (1991): 1135S-1140S.


Carpenter, Kenneth J. The history of scurvy and vitamin C. Cambridge University Press, 1988.


Hodges, Robert E., Eugene M. Baker, James Hood, HOWERDE E. SAUBERLICH, and STEVEN C. MARCH. "Experimental scurvy in man." The American Journal of Clinical Nutrition 22, no. 5 (1969): 535-548.


Ortner, Donald J., Whitney Butler, Jessica Cafarella, and Lauren Milligan. "Evidence of probable scurvy in subadults from archeological sites in North America." American Journal of Physical Anthropology 114, no. 4 (2001): 343-351.


Mussini, Emilio, John J. Hutton, and Sidney Udenfriend. "Collagen proline hydroxylase in wound healing, granuloma formation, scurvy, and growth." Science 157, no. 3791 (1967): 927-929. Fain, Olivier, Emmanuel Mathieu, and Michel Thomas. "Lesson of the week: Scurvy in patients with cancer." BMJ: British Medical Journal 316, no. 7145 (1998): 1661.


Williams, Roger J., and Gary Deason. "Individuality in vitamin C needs." Proceedings of the National Academy of Sciences 57, no. 6 (1967): 1638-1641.


Eddy, Walter H. "An improvement in the quantitative assay of the antiscurvy vitamin (C)." American Journal of Public Health and the Nations Health 19, no. 12 (1929): 1309-1320.

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