Vitamin B6Deficiency in the Rhesus Monkey

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Abstract
During the past six years, extensive studies of pyridoxine (vitamin B6) deficiency in the rhesus monkey (Macaca mulatta) have revealed pathologic alterations which suggest that deficiency of pyridoxine may be of importance in the pathogenesis of human disease. Some 40 animals have been studied. The animals were maintained on an essentially synthetic diet fed in tablet form containing 73 per cent sucrose, 18 per cent vitamin-free casein, 2 per cent corn oil, and the essential vitamins and minerals. Animals subjected to pyridoxine deficiency regularly develop alterations in blood vessels which bear a very close similarity to arteriosclerosis as it occurs spontaneously in man. The experimental lesions are closely analogous in character and distribution to those found in man. In the experimental animals, the vascular lesions develop after five to six months of complete deprivation of this essential nutrient. Other pathologic changes which frequently occur are fatty metamorphosis and cirrhosis of the liver. Comparable lesions have not been found in control animals or in those subjected to other nutritional deficiencies. In animals maintained for two years or longer on the synthetic diet and given inadequate supplements of vitamin B6, the incidence of dental caries in the second dentition is unusually high. Attention is called to the essentiality of vitamin B6 in metabolism, particularly of proteins. It is problematic whether or not the average daily intake of pyridoxine in man (1.5 mg) is adequate to meet the metabolic needs. The question arises whether or not long-term suboptimal intake of pyridoxine may be a contributory factor in the pathogenesis of the important human diseases-arteriosclerosis, dental caries, and cirrhosis of the liver. It is hoped that future investigations will supply an early answer to this important question.