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Effect of vitamin B12 deficiency on neurodevelopment in infants: current knowledge and possible mechanisms
Daphna K Dror1, Lindsay H Allen
1Department of Nutrition at the University of California Davis, Davis, California, USA. dkdror@ucdavis.edu
Insights
Severe vitamin B12 deficiency in infants causes neurological issues like developmental regression. Prompt supplementation rapidly reverses these symptoms, highlighting the critical role of vitamin B12 for infant neurological health.
Area of Science:
- Pediatric Neurology
- Nutritional Neuroscience
- Developmental Pediatrics
Background:
- Infantile vitamin B12 deficiency presents with severe neurological symptoms.
- Symptoms include irritability, failure to thrive, apathy, anorexia, and developmental regression.
- These symptoms are rapidly reversible with vitamin B12 supplementation.
Purpose of the Study:
- To review current knowledge on infantile vitamin B12 deficiency.
- To analyze case studies of infants born to mothers with pernicious anemia or vegetarian diets.
- To discuss potential mechanisms underlying deficiency manifestations.
Main Methods:
- Literature review of infantile vitamin B12 deficiency.
- Pooled analysis of case studies.
- Discussion of proposed pathophysiological mechanisms.
Main Results:
- Vitamin B12 deficiency causes significant neurological impairment in infants.
- Neurological symptoms respond quickly to vitamin B12 treatment.
- Potential mechanisms include effects on myelination, methylation, cytokine balance, and lactate accumulation.
Conclusions:
- Infantile vitamin B12 deficiency is a serious condition with profound neurological consequences.
- Early diagnosis and supplementation are crucial for recovery.
- Further research into the precise mechanisms is warranted.
Abstract:
Severe vitamin B(12) 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 the current knowledge concerning infantile vitamin B(12) 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.
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