maintaining or improving vitamin A status in lactating women (de Pee et al., 1995), preschool children (Jalal et al., 1998), and young children (Takyi, 1999). Vitamin A status, as determined by serum retinol concentration, was not improved in Indonesian lactating women after the consumption of dark green leafy vegetables (de Pee et al., 1995). These women had hemoglobin concentrations less than 13 mg/dL. There is evidence that iron deficiency impairs the metabolism of vitamin A in laboratory animals (Jang et al., 2000; Rosales et al., 1999). In some, but not all, studies (Suharno et al., 1993), iron supplementation improved vitamin A status in humans (Munoz et al., 2000). Therefore the presence of iron deficiency, which is prevalent in developing countries, may impair the efficacy of dark green leafy vegetables. Jalal and coworkers (1998) reported that the addition of β-carotene-rich foods to the diets of preschool children improved vitamin A status, however, vitamin A status improved almost as well when fat was added to the diet and an anthelmintic drug to destroy parasitic worms was provided. This finding demonstrates the importance of dietary fat, which is often low in the diets of developing countries and the importance of intestinal parasites on vitamin A status. Takyi (1999) reported that the vitamin A status of young children improved similarly when fed either a pureed β-carotene-rich diet or provided a similar amount of β-carotene as a supplement. Here, in contrast to the findings of Jalal et al. (1998), dietary fat and anthelmentic drugs did not appear to have a beneficial effect on vitamin A status, possibly because the carotenoid was already provided in a highly absorbable, pureed form.
The EARs that have been set for the North American population are achievable through diet because of the abundance of vitamin A-rich foods. Populations of less developed countries may have difficulty in meeting the EAR that ensures adequate vitamin A stores. Therefore, an EAR that does not assure adequate vitamin A stores has been determined on the basis of the level of vitamin A for correction of abnormal dark adaptation in adults. This approach does not assure adequate stores of vitamin A because animal studies indicate that vitamin A depletion of the eye occurs after the depletion of hepatic vitamin A reserves (Bankson et al., 1989; Lewis et al., 1942). Furthermore, epidemiological studies in children suggest impaired host resistance to infection, presumably reflecting compromised immunity and represented by increased risk of morbidity and mortality at lesser stages of depletion (Arroyave et al., 1979; Arthur et al., 1992; Barreto et al., 1994; Bloem et al., 1990; Ghana