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and Americans living in the East. It is more common among males than among 
females and it generally attacks individuals under 30 years of age. 
Manson’s theory as to the origin of beriberi is that the disease is a neuritis 
caused by a toxin, the latter being the product of a germ operating in some 
culture medium located outside of the human body. He believes that this toxin 
does not enter the body in food or in water but is inhaled or introduced through 
the skin. 
Takagi, late surgeon-general of the Japanese navy, still adheres to the theory 
that kakke is due to an insufficient diet, particularly to one containing a 
large amount of rice. When he first studied the question of the etiology of 
beriberi, the ratio of beriberi patients in the Japanese naval force in 1883 was 
231 per thousand. After the diet was changed, the number of kakke patients 
in this branch of the Japanese service diminished, so that in 1898 the ratio was 
only 0.87 per thousand. However, it has frequently been pointed out that during 
this period of time the number of kakke patients in Japan had also greatly 
diminished in districts and among bodies of men where such a radical change of 
diet had not taken place. 
Experiments on several hundred prisoners in the Malay Peninsula during a 
period of eleven months furnished conclusive proof to Wright that beriberi was 
contracted, even though the diet was qualitatively and quantitatively correct. 
He thinks that his experiments positively eliminate diet, as such, as a factor in 
the causation of the disease. 
Durham was struck by the fact that the well-to-do in and about the Federated 
Malay States escaped the disease, whereas people who were in poor surroundings 
were stricken, so that it was difficult not to believe that some food constituent, 
when sufficient in amount, protected the nervous system. However, he also 
noticed that beriberi may spread through a community in which the inhabitants 
are taking a sufficiently nitrogenous diet, and in proof of this he cites the 
instance of the prisoners in the gaol of the Federated Malay States. In spite 
of all, he thinks it is difficult, if not impossible, not to believe that the character 
of the food and the occurrence of beriberi are in some way related. Many of the 
published records seem to indicate such a connection, although the records of the 
Puda gaol show that the old theory of nitrogen starvation can not be upheld. 
Stanley (1. ¢.) remarks that in Shanghai, China, beriberi as a rule becomes 
prevalent toward the end of the summer. He saw 500 cases among the Chinese 
prisoners in the municipal gaol and in three police stations from 1898 until 1902. 
Most of these occurred among the long-term prisoners, in spite of the fact that 
they lived under better conditions as regards ventilation, cleanliness, exercise, 
and food than they did prior to their incarceration. Beriberi among the better 
classes of the general population is rare in Shanghai. Stanley declares that he 
is unable to answer the question why beriberi should be so much more prevalent 
among the municipal prisoners than it is among the general Chinese population 
of the city. 
Sambon * thinks that an enormous amount of evidence has been brought forward 
against the belief that rice diet is a direct causative factor in beriberi; how- 
ever, this diet may be related to beriberi just as we now understand the 
consumption of maize to be related to pellagra; but nevertheless, he believes that 
the specific agent of beriberi lives within the patient’s body. He finds the preva- 
lence of the disease to be increased by a high temperature and an abundant 
rainfall, and recalls that it is chiefly an affection of the common laborer, that we 
are absolutely ignorant of the manner in which it is carried from place to place, 
*Sambon: A Discussion on Beriberi. Brit. Med. Journ. (1902), 2, 835. 
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