BERIBERI

also called vitamin B1 deficiency, nutritional disorder caused by a deficiency of vitamin B1 (thiamine) and characterized by impairment of the nerves and heart. General symptoms include loss of appetite and overall lassitude, digestive irregularities, and a feeling of numbness and weakness in the limbs and extremities. (The term beriberi is derived from the Sinhalese word meaning extreme weakness.) In the form known as dry beriberi, there is a gradual degeneration of the long nerves, first of the legs and then of the arms, with associated atrophy of muscle and loss of reflexes. In wet beriberi, a more acute form, there is edema (overabundance of fluid in the tissues) resulting largely from cardiac failure and poor circulation. In infants breast-fed by mothers who are deficient in thiamine, beriberi may lead to rapidly progressing heart failure. The cardiac symptoms, in both infants and adults, generally respond promptly and dramatically to the administration of thiamine. When neurological involvement is present, response to thiamine therapy is much more gradual; in more severe cases, the structural lesions of the nerve cells may be irreversible. Thiamine normally plays an essential role as a coenzyme in the metabolism of carbohydrates; in its absence, pyruvic acid and lactic acid (products of carbohydrate digestion) accumulate in the tissues, where they are believed to be responsible for most of the neurological and cardiac manifestations. Vitamin B1 occurs widely in food but may be lost in the course of processing, particularly in the milling of grains. In East Asian countries, where polished white rice is a dietary staple, beriberi has been known for over 1,000 years. The history of the recognition, the cause, and the cure of beriberi is dramatic and is well documented in medical literature. In the 1870s the Japanese navy reported that beriberi had been eradicated among its sailors as a result of adding extra meat, fish, and vegetables to their regular diet. Before that time, almost half of the sailors were likely to develop beriberi, and many died of it. In 1897 Christiaan Eijkman, working in the Dutch East Indies (now Indonesia), showed that a beriberi-like disease could be produced in chickens by a diet of polished rice. That beriberi in humans was also related to the ingestion of white rice was confirmed by British researchers in Malaysia. There, W. Fletcher in 1907 and Henry Fraser and A.T. Stanton in 1909 showed that in selected groups under close observation beriberi occurred in persons who were eating a polished-rice diet whereas those eating parboiled or brown rice did not develop the disease. In 1912 Casimir Funk demonstrated that beriberi could be cured in pigeons by feeding them a concentrate made from rice polishings. Following this discovery he proposed that this, as well as several other conditions, were due to the ingestion of diets that were deficient in specific factors which he termed vitamines. The incidence of beriberi in Asia has markedly decreased, partly because an improved standard of living has allowed a more varied diet and partly because of the gradual popular acceptance of partially dehusked, parboiled, and enriched riceforms that contain higher concentrations of thiamine. The prevention of beriberi is accomplished by eating a well-balanced diet, since thiamine is present in most raw and untreated foods. In Western countries, thiamine deficiency is encountered almost solely in cases of chronic alcoholism.