From http://pediatrics.aappublications.or...ull/108/3/624:

Objective.* Cobalamin deficiency accompanied by bone marrow dysfunction and impaired central nervous system development has been reported in infants who were born to mothers with low cobalamin intake. We investigated the relation between cobalamin status in newborns and in their healthy mothers who consumed an omnivorous diet.

Methods.* Serum cobalamin and the functional markers plasma methylmalonic acid (MMA) and total homocysteine (tHcy) were determined in 173*newborns and their mothers. Forty-five children and mothers were reinvestigated after 6*weeks.

Results.* At birth, median (interquartile range) serum cobalamin levels were 245*(175-323) pmol/L in the mothers and 314*(238-468) pmol/L in the newborns. In the neonates, serum cobalamin, but not folate, was inversely associated with MMA and tHcy. Among maternal factors, low serum cobalamin was the strongest predictor of impaired cobalamin function (defined as low cobalamin, high tHcy, or high MMA levels) in the newborns. After 6*weeks, the maternal cobalamin levels had increased (to 421*[271-502] pmol/L), whereas the newborn levels had declined (to 230*[158-287] pmol/L). In the same interval, the infants had a marked increase in plasma MMA (from 0.29*[0.24-0.38] to 0.81*[0.37-1.68] Ámol/L). At 6*weeks, parity was a strong predictor of cobalamin status in the infant.

Conclusion.* The cobalamin status in the neonatal period is strongly associated with maternal cobalamin status and parity. A reduction in serum cobalamin and an increase in metabolite levels are consistent with impaired cobalamin function in a significant portion of the infants who were born to healthy, nonvegetarian mothers. *Key words:* newborn, infant, cobalamin, folate, homocysteine, methylmalonic acid.



There are several reports on cobalamin deficiency in children of mothers who are strict vegetarians.1,2 The propensity of infants who are born to mothers with low cobalamin intake to become deficient1,3 suggests that cobalamin status during infancy is critically dependent on fetal cobalamin accumulation and, thereby, maternal cobalamin status in pregnancy.


In infancy, impaired cobalamin function leads to dysfunction of the central nervous system.4,5 Severe clinical symptoms and neurologic deterioration have been documented in infants with nutritional cobalamin deficiency.6,7 In children from macrobiotic families, metabolic signs of persistent cobalamin deficiency were observed even in adolescence after consumption of animal products since the age of 6*years.8 Although these adolescents seemingly were in good health, clear evidence of impaired cognitive performance was demonstrated.9 This emphasizes the importance of cobalamin status for central nervous system development and shows that even moderate deficiency in children may be harmful.6,10


During the past decade, it was documented that impaired cobalamin status may exist with normal serum cobalamin and without the classical sign of megaloblastosis or neuropathy.11 This concept is based on studies that measure plasma levels of the metabolites methylmalonic acid (MMA) and total homocysteine (tHcy), which serve as markers of cobalamin function in tissues. Cobalamin functions as a cofactor in the enzymes methylmalonyl coenzyme A mutase and methionine synthase, and impaired catalytic activity of these enzymes causes accumulation of MMA and tHcy, respectively. MMA is a relatively specific indicator of cobalamin function, whereas increased tHcy is observed in a variety of conditions, including folate deficiency.12,13