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Common metabolic profile in infants indicating impaired cobalamin status responds to cobalamin supplementation

Anne-Lise Bjørke-Monsen1, Ingrid Torsvik, Hege Saetran

  • 1Department of Clinical Biochemistry, Haukeland University Hospital, N-5021 Bergen, Norway. almo@helse-bergen.no

Pediatrics
|July 4, 2008
PubMed

Insights

Infants often show signs of low vitamin B12 (cobalamin). Supplementation improved cobalamin levels and reduced harmful metabolites, indicating insufficient vitamin B12, not immature metabolism.

Area of Science:

  • Nutritional Biochemistry
  • Pediatric Metabolism
  • Vitamin B12 Metabolism

Background:

  • A significant proportion of breastfed infants exhibit a metabolic profile suggestive of impaired cobalamin (vitamin B12) status.
  • This metabolic profile is characterized by elevated levels of total homocysteine and methylmalonic acid.
  • The underlying cause in infants—whether immature organ systems or true cobalamin deficiency—remains a critical question.

Purpose of the Study:

  • To investigate the cause of the prevalent impaired cobalamin status observed in breastfed infants.
  • To determine if the observed metabolic profile reflects immature organ systems or insufficient cobalamin levels.
  • To assess the impact of cobalamin supplementation on key metabolic markers in infants.

Main Methods:

  • A single-center, randomized, placebo-controlled trial involving 107 six-week-old infants.
  • Infants were randomly assigned to receive either an intramuscular injection of 400 µg of cobalamin or a placebo.
  • Serum cobalamin and plasma concentrations of total homocysteine, methylmalonic acid, and cystathionine were measured at enrollment and at 4 months of age.

Main Results:

  • No significant differences in vitamin markers were observed between the cobalamin intervention and placebo groups at baseline (6 weeks).
  • At 4 months, infants receiving cobalamin supplementation showed a 75% increase in median serum cobalamin levels.
  • Cobalamin supplementation led to significant reductions in plasma total homocysteine and methylmalonic acid levels, while these remained unchanged in the control group.

Conclusions:

  • Cobalamin supplementation effectively normalized all markers associated with impaired cobalamin status in infants.
  • The study concludes that elevated total homocysteine and methylmalonic acid levels in a large fraction of infants are due to insufficient cobalamin, not immature metabolism.
  • These findings underscore the importance of adequate cobalamin status for supporting essential metabolic pathways in infants.
Abstract

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