American Journal of Clinical Nutrition, Vol 27, 470-478, Copyright © 1974 by The American Society for Clinical Nutrition, Inc.

Nutritional vitamin B₁₂ deficiency in rhesus monkeys

¹ From the Departments of Medicine and Neurology, Case Western Reserve University School of Medicine at Cleveland Metropolitan General Hospital, Cleveland, Ohio 44109

It has been reported that monkeys deprived of dietary vitamin B₁₂ have low serum levels and that some develop "cage-paralysis," i.e., demyelination of the posterior and lateral columns of the spinal cord resembling that in human subacute combined degeneration (SCD). To extend these findings under controlled conditions, 12 monkeys were fed a defined experimental diet that supplied less than 500 pg B₁₂ per day (8 were studied for 31 months, 4 for 20 months). Three monkeys received 20 µg B₁₂ intramuscularly every 14 days; three monkeys received supplemental folic acid. The deficient animals showed perisistently falling B₁₂ levels in serum (to 10 pg/ml by 13 months) and RBC (to 72 pg/ml by 20 months). At 21 months, hepatic B₁₂ levels were 5% of controls. After 16 months all deficient animals (but no controls) excreted abnormal amounts of methylmalonic acid. Assays of folate, B₆, iron, ascorbic acid, vitamin E, and trace metals were used to exclude or correct other dietary deficiencies. The monkeys have normal growth rates, appear healthy, and behave normally. Eight to 15 months after marked B₁₂ deficiency was documented, peripheral blood and bone marrow show no abnormalities nor is there clinical evidence of SCD.