al., 1985). Darkly pigmented infants require a greater exposure to sunshine to initiate the synthesis of vitamin D in the skin (Clemens et al., 1982).
In a study by Greer and colleagues (1982), which included randomization of breastfed infants to a placebo or to a daily supplement of 10 µg of vitamin D, the bone mineral content of the placebo group was significantly lower in the first few months after birth but slightly higher than that of the supplemented group by the end of the first year.
In summary, exclusive breastfeeding results in normal infant bone mineral content when maternal vitamin D status is adequate and the infant is regularly exposed to sunlight. If the infant or mother is not exposed regularly to sunlight, or if the mother's intake of vitamin D is low, supplements for the infant may be indicated (5 to 7.5 µg/day).
Although vitamin A concentrations in human milk are dependent on the mother's vitamin A status, vitamin A deficiency is rare among breastfed infants, even in parts of the world with endemic vitamin A deficiency (Sommer, 1982). Even after breastfeeding is discontinued, it appears to confer a protective effect (Sommer, 1982; West et al., 1986), presumably because some of the vitamin A provided by human milk is stored in the liver. Infants who consume human milk that provides 100 to 151 µg of retinol equivalents per day grow well and do not show signs of vitamin A deficiency. In the United States, human milk provides approximately twice this amount (FAO, 1988; NRC, 1989). These U.S. concentrations are used as the international standard for adequate vitamin A intakes in infancy (FAO, 1988; NRC, 1989). In the United States, there is no indication to routinely supplement either the infant or the mother with vitamin A.
Vitamin K is essential for the formation of several proteins required for blood clotting. This vitamin has two major forms: vitamin K1 (phylloquinone), synthesized by plants, and vitamin K2 (menaquinone), synthesized by bacteria. Most of the vitamin K in human milk is phylloquinone; the extent to which infants absorb menaquinone produced by gut microflora is not known. Vitamin K stores at birth are extremely low. Therefore, newborns are immediately dependent on an external source of the vitamin, but the amount provided by human milk is low—approximately 2 µg/liter (Committee on Nutrition, 1985; NRC, 1989). Bacteria that colonize the intestinal tracts of breastfed infants produce less menaquinone than do those in formula-fed infants.
A deficiency of the vitamin produces a syndrome in infants called hemorrhagic disease of the newborn. This vitamin K-dependent disease has two different clinical forms. The classic early-onset form occurs at age 2 to 10