Epidemiology and Etiology

Observations about pellagra made in Spain in the early eighteenth century have stood the test of time: The disease is associated with a maize diet and occurs mainly among the poor. These observations were repeated over the years, and their scientific validity was confirmed more than 200 years later by work done in the United States during the second and third decades of the twentieth century.

The U.S. Public Health Service, working in the southern states, linked pellagra conclusively to the peculiar "3 M" diet of the region - meat, meal, and molasses - and to the poverty of which this diet was a symbol. Bread made from cornmeal was the largest component of the pellagrin's daily fare. Meat was pork fat back, and molasses was syrup made from cane. Widespread pellagra was found among tenant farmers and mill workers, in orphanages and mental institutions. The diet of pellagrins was always both monotonous and cheap. In what would become one of the classic studies in epidemiology, pellagra was linked irrevocably to economics. A systematic analysis of diet in relation to the income of workers in South Carolina mill villages showed that pellagra appeared wherever income was marginal and variety in diet was limited.

The missing element in the pellagrin's diet at first was called the pellagra-preventing or "P-P" factor. Although its exact nature was unknown, it was proved to exist in a number of foods including meat, milk, eggs, and certain vegetables, particularly turnip greens. One of the richest and least expensive sources was found in yeast. In 1937, the P-P factor was identified specifically as nicotinic acid, or niacin, a B-complex vitamin. Adding niacin to the diet almost magically eliminates even the worst symptoms of pellagra.

The discovery of niacin as the pellagra-preventive factor, however, did not answer all the questions about the disease. It did not explain why milk, a poor source of niacin, would prevent pellagra, nor why a diet based mostly on corn, which possesses more niacin than milk, causes it. The answer to part of the riddle lay in the discovery that the liver can convert the amino acid tryptophan, of which milk is a rich source, into niacin. The mystery of corn's association with pellagra lies in the type of niacin it contains.

Niacin is distributed in a wide variety of foods including cereals, legumes, oilseeds, meat, tea, and coffee. Its presence in food, however, does not mean that it is always available to the body. Niacin may appear in a free form ready to be absorbed; or it may appear in a bound form called niacytin and be biologically unavailable, as is the case with maize. Niacytin is released only after the grain is treated with an alkali such as lime. In Mexico and Central America, where pellagra has seldom been a problem even though corn is the dietary staple, the grain is soaked in lime and heated before being baked as tortillas. Treatment with lime also lowers the content of the amino acid leucine in corn.

It is the high leucine content of millet jowar (Sorghum vulgare) that is thought to be responsible for the appearance of pellagra in Egypt and India where this grain constitutes a large part of the diet. Niacin is found in jowar in a free form and is therefore nutritionally available, but the grain's protein has an imbalance between leucine and the amino acid isoleucine. Like maize, jowar contains a relative excess of leucine, about 12 percent, as compared with a level of below 8 percent in most other cereals. This excess brings about a conditioned niacin deficiency, one in which pyridoxine, vitamin B6, appears to play a role.

The amount of niacin required in the diet is affected by the quality of protein consumed because tryptophan is a precursor of niacin. The term niacin equivalent is used because 60 milligrams of tryptophan supply 1 milligram of niacin. An adequate diet contains 6 to 9 milligrams of niacin-equivalents per day for infants, 11 to 18 for children, and 13 to 19 for adults.

Thus the etiology of pellagra is incredibly complex. The disease may result from either a niacin deficiency or an amino acid imbalance. Three essential amino acids - tryptophan, leucine, and isoleucine -and two vitamins - niacin and vitamin B6 — are involved. The interaction of these nutrients is not fully understood, and other nutrients as well as hormones may have a role. There is also an apparent association of pellagra with sunshine.

Regular consumption of alcohol is related to the development of pellagra, as are parasitic infections, particularly schistosomiasis. Pellagra also may be precipitated by treatment with certain drugs. Iso-niazid, used to treat tuberculosis, and 3-mercapto-purine, used to treat leukemia, can lead to a niacin deficiency. In patients with malignant carcinoid, tryptophan is diverted mainly to serotonin rather than to niacin, and pellagra may follow. Hartnup's disease, a genetic disorder that causes errors in tryptophan metabolism, looks much like pellagra and is responsive to niacin therapy.

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