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ARS Home » Pacific West Area » Davis, California » Western Human Nutrition Research Center » Obesity and Metabolism Research » Research » Publications at this Location » Publication #221772
Title: Effect of vitamin B12 deficiency on neurodevelopment in infants: current knowledge and possible mechanisms

Author
item DROR, DAPHNA - UCD, NUTR. DEPT.
item Allen, Lindsay - A

Submitted to: Nutrition Reviews
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/1/2007
Publication Date: 5/1/2008
Citation: Dror, D.K., Allen, L.H. 2008. Effect of vitamin B12 deficiency on neurodevelopment in infants: current knowledge and possible mechanisms. Nutrition Reviews. 66(5):250-255, 2008.

Interpretive Summary: Vitamin B12 deficiency has adverse effects on infant development that are often permanent. Most information on this topic has been published as case studies of individual breastfed infants whose mothers were B12 deficient because they consumed strictly vegetarian diets or had undiagnosed pernicious anemia (vitamin B12 malabsorption). Infants of these mothers are born with low B12 stores and are fed with breast milk deficient in the vitamin. We pooled the data from 30 case studies of infants diagnosed with B12 deficiency due to maternal vegetarianism, and 18 case studies of infants whose mothers had undiagnosed pernicious anemia. Symptoms are similar in both groups, and include megaloblastic anemia, refusal of complementary foods, poor muscle tone, developmental delays, and low weight, height and head circumference. Injecting the infants with a high dose of B12 improves many of these symptoms within days or weeks, although permanent damage may occur. The rapid recovery means that poor nerve fiber myelination is unlikely to be the sole cause of the symptoms. Newer data suggest other underlying causes including altered biochemical and immunological processes.

Technical Abstract: Severe vitamin B12 deficiency produces a cluster of neurological symptoms in infants, including irritability, failure to thrive, apathy, anorexia, and developmental regression, which respond remarkably rapidly to supplementation. The underlying mechanisms may involve delayed myelination or demyelination of nerves; alteration in the S-adenosylmethionine:S-adenosylhomocysteine ratio; imbalance of neurotrophic and neurotoxic cytokines; and/or accumulation of lactate in brain cells. This review summarizes current knowledge concerning infantile vitamin B12 deficiency, including a pooled analysis of case studies of infants born to mothers with untreated pernicious anemia or a strict vegetarian lifestyle and a discussion of the mechanisms that may underlie the manifestations of deficiency.