The disease of beriberi has been common in the Orient for many years. The Malay States, Siam, Corea, parts of Japan, and the Philippines have all been extensively afflicted with it Hoist1 reports that of the ships arriving at Falmouth in the year 1900 from harbors south of 33° North, 0.5 per cent of the English ships and nine per cent of the Norwegian ships had cases of beriberi on board. Reports of the disease have come from India, Africa,2 Marseilles,3 and Spain.4 According to Fraga,5 epidemics have frequently been reported in Brazil, although often under other names. The first serious outbreak in North America was reported by Little in Newfoundland and Labrador in 1912,* but occasional cases have been reported from time to time in the South and West of the United States.7

Simpson8 has reported some interesting observations which seem to indicate that natives of certain localities may show a greater predisposition than others to this disease. Of different nationalities admitted to the beriberi hospital in Singapore, Chinese were six times as numerous as all others.9 While the disease in its true form is of common occurrence among recent immigrant Chinese, it is practically unknown among Straits-born settlers in the colony. The disease is most prevalent among the coolie class, those employed on rubber estates being especially prone to infection. Certain areas in Johore were constantly found to furnish the largest number of patients. During the same period, of a considerable number of sawmill coolies admitted from a wide area no less than three-quarters were found to have come from one mill. Of those employed at different trades, tailors alone accounted for more than half. Inquiries into former dietaries of a considerable number of beriberi patients, particularly as to the consumption of polished rice, showed no outstanding differences between them and that of the Straits Chinese, who did not appear to suffer from the disease in its true form.

1 Hoist, Tr. 8oc. Trop. Med. Hyg. 5, 76. See also Hoist and Frdlich, Z. f. Hyg. Infekt. 72, 1, 1912.

2 Wydooghe, Bull. Soo. Path. Exot. March, 1918. Quoted by Jelliffe, J. Nerv. Ment. Dis. 49, 522, 1919.

3 Sicard, Roger, and Rimbaud, Paris Med. Dec. 1, 1917. 4 Vinson, Bull. Soc. Med. Maur. 1917.

5 Fraga, New, Orl. Med. Surg. J. 1918.

6 Little, J. Am. Med. Am. 58, 2029, 1912; 63, 1287, 1914.

7 For further details as to the topographical incidence of beriberi see Jelliffe, 1. c.

8 Simpson, Lancet, 1919, ii, 1027.

9 Japanese, Javanese, Malays, and Indians.

In this connection reference may be made to the suggestion of De Langen and Schut,10 that the liability of inhabitants of the tropics to certain diseases may be due to the excessively high content of sugar in the blood. A defective diet, they state, which in temperate climates would not be sufficiently deficient in vitamin to cause beriberi, might also in this way, in the tropics, induce that disease.

A high incidence of beriberi among women is reported in the Philippines, especially among mothers who are suckling babies. These women were found to be suffering from undernourishment, polished rice forming the greater part of their dietary. Their breast milk is poor in quality, to which is attributed the occurrence of beriberi in infants. Andrews induced several Filipino women whose infants had just died of beriberi to nurse young pups, and noted that in all cases the latter failed to grow, because edoematous, and lost the use of their hind legs.

Chemical analysis shows that human milk in beriberi differs very little in composition from the normal11 but it is lacking in the anti-neuritic substance which is present in normal milk. Hirota12 reports a few cases of beriberi in breast-fed infants whose mothers did not suffer from the disease, which can only be explained on the theory that through some abnormality the essential factor was not secreted by the mammary gland, although present in sufficient quantity for the normal metabolism of the mothers.

Beriberi was originally regarded as an infection, flourishing in insanitary surroundings, but in 1880 Takaki, Inspector General of the Japanese navy, carried out an investigation which discredited this theory and pointed to a purely dietetic origin. Takaki found that as far as sanitary conditions were concerned the ships of the Japanese navy which were ravaged by this disease compared favorably with the European ships which were entirely free from it. The only pronounced difference between the Japanese and the European hygiene was to be found in the food, the Japanese ration at that time containing a much larger proportion of carbohydrate food, which was almost entirely in the form of polished rice. Just at this time a Japanese vessel had made a nine-months' cruise from Japan to New Zealand, Valparaiso, and Honolulu. Out of the 276 men on board 169 had developed beriberi, 25 cases being fatal. Takaki sent a second vessel over the same route with a similar crew and identical conditions except that a part of the rice ration was replaced by barley, vegetables, meat, and condensed milk. At the end of the cruise only 14 cases of beriberi had been reported, and these were all men who had refused to eat their allowance of the new foods.

As a result of this test the character of the ration throughout the Japanese navy was gradually changed, in spite of the difficulty of educating the sailors to new dietary habits, with the gratifying result that beriberi almost disappeared. Whereas previous to 1884 nearly 33 per cent of the marines suffered from beriberi, during the six years after the adoption of the new diet, only 16 per cent were affected, and later the number of cases was reduced to two or three a year.13 This beneficial effect was ascribed by the Japanese authorities to the increased amount of protein in the new diet, but strange to say neither the observed facts nor the explanation made much impression on medical opinion, according to which the disease was still to be regarded as an infection, despite the fact that all efforts to check it by improved sanitation proved unavailing.

10 De Langen and Schut, Geneesk. Tidjschr. v. Neder-Indie 56, 490, 1016. Trop. Dis. Bull. 9, 259, 1917.

11 Andrews, Phil. J. 8ci. 7B, 67.

12 Hirota, Zent. f. inn. Med. 16, 385.

13 Oshima, Bull. 150, Office of Exp. Sta. U. S. Dept. Agric. 1906.