Background

Vitamin B12, often referred to as cobalamin, is required for the formation of red blood cells and normal neurological function [62]. Similar to folate, vitamin B12 is involved in DNA synthesis. If vitamin B12 deficiency occurs, then DNA production is disrupted, producing megaloblastic changes in blood cells (macrocytosis). Neurological complications occur in 75-90% of individuals with clinically defined vitamin B12 deficiency [62]. When a deficiency occurs in developed countries, it is frequently associated with inadequate absorption rather than a dietary deficiency. Inadequate absorption could be caused by chronic antacid use, atrophic gastritis, hypochlorhydria, or pernicious anemia—most frequently found in individuals >50 years of age.

High doses of synthetic folic acid (greater than 1,000 mcg) can mask vitamin B12 deficiency by reversing megaloblastic anemia [63, 72]. Megaloblastic anemia is the clinical indicator that often leads a clinician to suspect that vitamin B12 deficiency may be an issue. Vitamin B12 is excreted in the bile and effectively reabsorbed such that it can take up to 20 years for a vitamin B12 deficiency to develop due to low vitamin B12 intake. In contrast, a deficiency due to poor absorption can take only a few years to develop.

During lactation, the concentration of vitamin B12 in human milk varies widely, and reflects maternal vitamin B12 intake and status [62]. Low maternal intake or poor absorption of vitamin B12 rapidly leads to a low level of vitamin B12 in human milk [73]. Severe deficiency can occur after approximately 4 months of age in exclusively breast-fed infants of mothers with inadequate intake [74]. It is postulated the rapid postnatal development of vitamin B12 deficiency in the infant is due, in part, to poor in utero transfer of vitamin B12 from mother to child. Simply put, if a mother's vitamin B12 status is suboptimal in lactation, it could very well have been in pregnancy as well. Symptoms of infantile vitamin B12 deficiency include irritability, abnormal reflexes, feeding difficulties, reduced level of alertness or consciousness leading to coma, and permanent development disabilities if diagnosis is delayed [75].

Despite woman-to-woman variation in milk vitamin B12 content, the concentration of vitamin B12 in human milk changes very little after the first month postpartum [76]. The average reported concentration of vitamin B12 secreted in the milk of well-nourished mothers is approximately 0.33 mcg/day during the first 6 months of lactation, and 0.25 mcg/day during the second 6 months [76]. In a group of women receiving vitamin B12 containing supplements, the average B12 content of milk was 0.91 mcg/l [77], while the B12 content of milk from unsupplemented vegetarian mothers was lower, averaging 0.31 mcg/l [73].

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