No adverse effects are observed in adults with dietary calcium intakes of 2.5 g/day. There is concern that higher intakes may increase the risk of urinary stone formation, constipation, and decreased renal function and may inhibit intestinal absorption of other minerals (iron, zinc).
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Gastrointestinal Bleeding Anemia Failure to Thrive
Iron, the most abundant trace mineral, is used in the synthesis of hemoglobin, myoglobin, and enzyme iron. Bodyiron content is regulated primarily through modulation ofiron absorption, which depends on the state of body ironstores, the form and amount of iron in foods, and the mixture of foods in the diet. There are two categories of ironin food. The first is heme iron, present in hemoglobin and myoglobin, which is supplied by meat and rarely accountsfor more than one fourth of the iron ingested by infants.The absorption of heme iron is relatively efficient and is notinfluenced by other constituents of the diet. The second category is nonheme iron, which represents the preponderanceof iron intake consumed by infants and exists in the formof iron salts. The absorption of nonheme iron is influencedby the composition of consumed foods. Enhancers of non-heme iron absorption are ascorbic acid, meat, fish, and poultry. Inhibitors are bran, polyphenols (including the tannatesin tea), and phytic acid, a compound found in legumes andwhole grains. The percent intestinal absorption of the smallamount of iron in human milk is 10%; 4% is absorbed from iron-fortified cow’s milk formula and from iron-fortified infant dry cereals.
In a normal term infant, there is little change in total bodyiron and little need for exogenous iron before 4 months ofage. Iron deficiency is rare in term infants during the first4 months, unless there has been substantial blood loss (seeChapter 62). After about 4 months of age, iron reserves become marginal, and, unless exogenous sources of iron areprovided, the infant becomes progressively at risk for anemiaas the iron requirement to support erythropoiesis and growthincreases (see Chapter 150). Premature or low birth weightinfants have a lower amount of stored iron because significantamounts of iron are transferred from the mother in the third trimester. In addition, their postnatal iron needs are greaterbecause of rapid rates of growth and when frequent phlebotomy occurs. Iron needs can be met by supplementation(ferrous sulfate) or by iron-containing complementary foods.Under normal circumstances, iron-fortified formula should be the only alternative to breast milk in infants younger than1 year of age. Premature infants fed human milk may developiron deficiency anemia earlier unless they receive iron supplements. Formula-fed preterm infants should receive iron-fortified formula.
In older children, iron deficiency may result from inadequate iron intake with excessive cow’s milk intake or from intake of foods with poor iron bioavailability. Iron deficiency also can result from blood loss from such sources as menses or gastric ulceration. Iron deficiency affects many tissues (muscle and central nervous system) in addition to producing anemia. Iron deficiency and anemia have been associated with lethargy and decreased work capacity and impaired neurocognitive development, the deficits of which may be irreversible when onset is in the first 2 years of life.
The diagnosis of iron deficiency anemia is established by the presence of a microcytic hypochromic anemia, low serum ferritin levels, low serum iron levels, reduced transferrin saturation, normal to elevated red blood cell width distribution, and enhanced iron-binding capacity. The mean corpuscular volume and red blood cell indices are reduced, and the reticulocyte count is low. Iron deficiency may be present without anemia. Clinical manifestations are noted in Table 31-4.