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Vitamin B12 Essential for Infant Brain Development, PGI Study Finds - Video
Overview
A new study from the Postgraduate Institute of Medical Education and Research (PGI) underscores the critical role of Vitamin B12 in infant brain development. Published in Pediatric Neurology, examined 141 infants diagnosed with B12 deficiency using MRI scans and standardized developmental assessments.
The findings revealed that affected infants commonly presented with delayed or regressed developmental milestones, lethargy, anaemia, tremors, and, in severe cases, darkened skin and light-coloured hair. Notably, many babies were not underweight, which can create a false sense of reassurance about their health. Nearly 60% showed reduced brain volume, reflected in poor head growth.
Encouragingly, after Vitamin B12 treatment, many infants demonstrated rapid improvement in alertness and developmental progress, highlighting the vitamin’s therapeutic potential. However, researchers cautioned that while early intervention can reverse many symptoms, long-term effects on learning, intellect, and behaviour may persist if treatment is delayed.
Lead author Naveen Sankhyam explained that Vitamin B12 is essential for red blood cell formation, DNA synthesis, and nervous system health. It plays a key role in myelin production—the protective covering around nerves that enables efficient brain signaling—making it especially crucial during the first year of life, when rapid brain growth occurs.
The study also points to India’s high risk profile, particularly among vegetarian mothers and exclusively breastfed infants of B12-deficient women. Since natural B12 sources are primarily animal-based, awareness, supplementation, and food fortification are vital public health strategies to prevent this entirely avoidable cause of long-term cognitive impairment.
REFERENCE: Pawan Kumar, Naveen Sankhyan, et al.; Neurological Consequences of Infantile Vitamin B12 Deficiency — A Prospective Cohort Study; Pediatric Neurology, Volume 177, 85 – 94; DOI: 10.1016/j.pediatrneurol.2025.12.012


