Chemistry Reference
In-Depth Information
hemoglobin concentration and high iron stores in the newborn (Food and
Nutrition Board: Institute of Medicine, 2001). Maternal iron deficiency is not
associated with neonatal iron-deficiency anemia but neonatal iron stores are
reduced (Kelleher and Lonnerdal, 2005), which puts the newborn at increased
risk for iron deficiency if they do not consume adequate amounts of iron-rich
complementary foods after 4-6 months of age (Domellof et al., 2002). Reg-
ulation of iron absorption changes between 6 and 9 months of age that
apparently enhances the ability of the infant to adapt to a low-iron diet.
That is, fractional iron absorption from breast milk can double between 6 and
9 months of age in infants not supplemented with iron. Thus, some infants
can avoid iron deficiency despite low-iron intake in late infancy (Domellof
et al., 2002). Men have higher iron stores than women and the requirement for
iron is much higher for reproductive-age females than any other sex-age
group. This is a reflection of the additional iron requirement associated
with menstrual blood loss (Food and Nutrition Board: Institute of Medicine,
2001). The iron requirement increases considerably for lactoovovegetarians
compared to non-vegetarians because non-heme iron absorption is consider-
ably lower in the former (Hunt and Roughead, 1999).
Heme iron is highly bioavailable, is soluble in the alkaline luminal
environment (such that binding proteins are not necessary for luminal
absorption) and enters the intestinal cell intact. On the other hand, non-
heme iron absorption depends on the solubilization of predominately ferric
food iron in the acid milieu of the stomach and subsequent reduction to the
ferrous form (Beard, 2006). This reduction is dependent upon interaction
with endogenous compounds such as a ferrireductase (present at the mucosal
surface of duodenal enterocytes) (Han et al., 1995) and dietary ascorbic acid
(Food and Nutrition Board: Institute of Medicine, 2001). Because mammals
lack a regulated pathway for iron excretion, iron homeostasis is regulated
primarily by iron absorption by duodenal mucosal cells. The hepatic anti-
microbial peptide, hepcidin, plays a key role in the negative feedback regula-
tion of intestinal iron absorption (Ward and Conneely, 2004).
The iron concentration in breast milk is probably under homeostatic
control because anemic women as well as women taking iron supplements
have levels of iron in their milk that are similar to those of non-anemic women
(Lonnerdal, 1997). Prematurity does not affect human milk iron concentra-
tions (Hunt et al., 2004). Maternal dietary iron supplementation with up to
30 mg of iron per day does not affect its concentration in milk (Siimes et al.,
1984). Apparent homeostatic control of iron in breast milk is probably
achieved by up- and down-regulation of transferrin receptors in the mam-
mary gland such that in a situation of maternal iron deficiency, a higher
number of mammary transferrin receptors facilitates the uptake of iron into
the gland and ensures a normal iron level in the milk (Lonnerdal, 1997).
