Few cases were reported in this country prior to 1907, when it was found to be present at the Columbia, South Carolina, State Hospital by Babcock. Pellagra constituted seven per cent of the admissions to that institution in 1908, fifteen per cent in 1909, twenty in 1910, over twenty-seven in 1911 and twenty-six per cent in 1915. Sixty-one per cent of the deaths in the hospital during the latter year were due to that disease. The health officer of the state reported four hundred cases in South Carolina in 1909 and six thousand in 1914. Babcock is now of the opinion that pellagra undoubtedly existed for twenty years or more at Columbia before its significance was known. In 1910 the disease was found to be present in thirty different states and represented about three thousand cases.[243] Of these the largest numbers were in Virginia, North Carolina, South Carolina, Georgia, Alabama, Mississippi, Louisiana, Texas, and Illinois. The importance of this question had already been recognized and a national conference was held on the subject at Columbia in 1909. During the same year the governor of Illinois appointed a commission to make a thorough study of pellagra in that state. The disease has been made the subject of elaborate investigation and study by the United States Public Health Service and several publications have been issued by that department.[244]
Notwithstanding the extended discussion and scientific research of the last few years, the question as to the definite etiology of pellagra has not as yet been positively settled. The maize or Indian corn theory was first advocated by Mazari in 1810. He believed the symptoms to be due to a deficiency in gluten. Sette in 1826 attributed the disease to a fungus (scimelpige) growing on corn and producing a poison from the oil in the grain. The smut of corn, "Ustilago Maydis," was suggested as a possible factor by Pari in 1860. In 1872 Lombroso formulated his toxic theory: "In pellagra we are dealing with an intoxication produced by poisons developed in spoiled corn through the action of certain microorganisms, in themselves harmless to man." He also announced the discovery of "pellagrosein," a toxic substance extracted from spoiled corn. In 1902 Ceni advanced the theory that the disease was caused by the action of certain moulds such as the aspergillus fumigatus and flavescens. The Illinois Pellagra Commission in 1911 came to the conclusion after an elaborate investigation of the subject that the primary etiological factor involved was a living microorganism of unknown nature, that the probable source of infection was through the intestinal tract and that a deficient amount of animal protein in the diet probably acted as a predisposing cause. Funk in 1914 suggested a vitamin deficiency in the diet brought about by the consumption of overmilled corn. Voegtlin[245] in the same year expressed the opinion that the disease was essentially a chronic intoxication,—"While the agents at work in this intoxication are as yet unknown, I am inclined to believe that toxic substances exist in certain vegetable foods, not necessarily spoiled, which, if consumed by man over a long period of time, may produce an injurious effect on certain organs of the body.... It is probably more than a mere coincidence that the population of that part of the world in which pellagra is endemic lives on a mainly vegetable diet."
In 1916 a study was made by Koch and Voegtlin[246] of the chemical changes found in the nervous system in pellagra which was very significant in its results. They found an increase in water with a decrease in proteins and lipoids, the latter reaction being attributed to a degeneration in the white matter. There was also a relative increase in the cholesterol content, looked upon as a compensatory protective function tending to replace the loss in lipoids. The most marked chemical alterations were found in the cord. On feeding monkeys and rats with an exclusive vegetable diet, changes in the chemical reaction of the brain and cord of almost exactly the same type were brought about experimentally.
Goldberger[247] in 1916 made an interesting report of a series of investigations carried on by the United States Public Health Service at Jackson, Mississippi. A large number of cases of pellagra were treated by largely supplementing the dietary with fresh meats, milk and leguminous vegetables. The carbohydrate content was reduced at the same time but corn was not entirely discontinued. Of 209 cases studied, 172 remained under continuous observation with a recurrence of symptoms in only one case. In a similar experiment made at the Georgia State Sanitarium seventy-two patients, all of whom had shown attacks previously, were treated for a year without symptoms. A number of volunteers at the Mississippi State Penitentiary were given a test diet consisting of wheat flour, corn meal, grits, cornstarch, white polished rice, granulated sugar, cane syrup, sweet potatoes, pork fat, cabbage, collards, turnip greens and coffee. Of the eleven convicts receiving this diet, six developed a typical dermatitis with slight nervous and gastrointestinal symptoms. The results of these investigations were not offered by the United States Public Health Service as being conclusive and incontrovertible evidence as to the etiology of pellagra, which must still be looked upon as being somewhat in doubt. The dietetic factors concerned in the production of the disease have been under serious consideration for a century or more.
This information was supplemented by a study of pellagra in the general population of the cotton mill communities in South Carolina.[248] In comparing the dietaries of pellagrous households with those of the families escaping infection it was found that the former consumed less meat, milk, butter, cheese and eggs. The value of their diet in calories and proteins was lower. The proteins contributed, moreover, were more largely from cereals, peas, beans, etc. The carbohydrate content was also lower. They concluded that the particular points involved were:—
"1. A physiologically defective protein supply,
"2. A low or inadequate supply of fat-soluble vitamin,
"3. A low or inadequate supply of water-soluble vitamin, and
"4. A defective mineral supply."
They were also of the opinion that the disease could be prevented by "including in the diet an adequate supply of animal protein foods (particularly milk, including butter, and lean meat)."