The objectives of this study were to quantify the effectiveness of dietary retinol sources, orange fruit, and dark-green, leafy vegetables in improving vitamin A status, and to test whether orange fruit is a better source of vitamin A and carotenoids than are leafy vegetables. Anemic schoolchildren aged 7-11 y (n = 238) in West Java, Indonesia, were randomly allocated to 1 of 4 groups to consume 2 complete meals/d, 6 d/wk, for 9 wk: 1) 556 retinol equivalents (RE)/d from retinol-rich food (n = 48); 2) 509 RE/d from fruit (n = 49); 3) 684 RE/d from dark-green, leafy vegetables and carrots (n = 45); and 4) 44 RE/d from low-retinol, low-carotene food (n = 46). Mean changes in serum retinol concentrations of the retinol-rich, fruit, vegetable, and low-retinol, low-carotene groups were 0.23 (95% CI: 0.18, 0.28), 0.12 (0.06, 0.18), 0.07 (0.03,0.11), and 0.00 (-0.06, 0.05) micromol/L, respectively. Mean changes in serum beta-carotene concentrations in the vegetable and fruit groups were 0.14 (0.12, 0.17) and 0.52 (0.43, 0.60) micromol/L, respectively. Until now, it has been assumed that 6 microg dietary beta-carotene is equivalent to 1 RE. On the basis of this study, however, the equivalent of 1 RE would be 12 microg beta-carotene (95% CI: 6 microg, 29 microg) for fruit and 26 microg beta-carotene (95% CI: 13 microg, 76 microg) for leafy vegetables and carrots. Thus, the apparent mean vitamin A activity of carotenoids in fruit and in leafy vegetables and carrots was 50% (95% CI: 21%, 100%) and 23% (95% CI: 8%, 46%) of that assumed, respectively. This has important implications for choosing strategies for controlling vitamin A deficiency. Research should be directed toward ways of improving bioavailability and bioconversion of dietary carotenoids, focusing on factors such as intestinal parasites, absorption inhibitors, and food matrixes.
There is little evidence to support the general assumption that dietary carotenoids can improve vitamin A status. We investigated in Bogor District, West Java, Indonesia, the effect of an additional daily portion of dark-green leafy vegetables on vitamin A and iron status in women with low haemoglobin concentrations (< 130 g/L) who were breastfeeding a child of 3-17 months. Every day for 12 weeks one group (n = 57) received stir-fried vegetables, a second (n = 62) received a wafer enriched with beta-carotene, iron, vitamin C, and folic acid, and a third (n = 56) received a non-enriched wafer to control for additional energy intake. The vegetable supplement and the enriched wafer contained 3.5 mg beta-carotene, 5.2 mg and 4.8 mg iron, and 7.8 g and 4.4 g fat, respectively. Assignment to vegetable or wafer groups was by village. Wafers were distributed double-masked. In the enriched-wafer group there were increases in serum retinol (mean increase 0.32 [95% CI 0.23-0.40] mumol/L), breastmilk retinol (0.59 [0.35-0.84] mumol/L), and serum beta-carotene (0.73 [0.59-0.88] mumol/L). These changes differed significantly from those in the other two groups, in which the only significant changes were small increases in breastmilk retinol in the control-wafer group (0.16 [0.02-0.30] mumol/L) and in serum beta-carotene in the vegetable group (0.03 [0-0.06] mumol/L). Changes in iron status were similar in all three groups. An additional daily portion of dark-green leafy vegetables did not improve vitamin A status, whereas a similar amount of beta-carotene from a simpler matrix produced a strong improvement. These results suggest that the approach to combating vitamin A deficiency by increases in the consumption of provitamin A carotenoids from vegetables should be re-examined.
Many indicators of micronutrient status change during infection because of the acute phase response. In this study, relationships between the acute phase response, assessed by measuring concentrations of C-reactive protein (CRP), alpha(1)-antichymotrypsin (ACT) and alpha(1)-acid glycoprotein (AGP), and indicators of micronutrient status were analyzed in 418 infants who completed a 6-mo randomized, double-blind, placebo-controlled, supplementation trial with iron, zinc and/or beta-carotene. The acute phase response, defined by raised CRP (plasma concentration >10 mg/L), raised AGP (>1.2 g/L), or both raised CRP and AGP, significantly affected indicators of iron, vitamin A and zinc status, independently of the effects of supplementation. Plasma ferritin concentrations were higher by 15.7 (raised AGP) to 21.2 (raised CRP and AGP) micro g/L in infants with elevated acute phase proteins compared with infants without acute phase response (P < 0.001). In contrast, plasma concentrations of retinol were lower by 0.07 (P < 0.05, raised AGP) to 0.12 (P < 0.01, raised CRP) micro mol/L, and of zinc lower by 1.49 (P < 0.01, raised AGP) to 1.89 (P < 0.05, raised CRP and AGP) micro mol/L. Hemoglobin concentrations and the modified relative dose response were not affected. Consequently, the prevalence of iron deficiency anemia was underestimated in infants with raised acute phase proteins by >15%, whereas the prevalence of vitamin A deficiency was overestimated by >16% compared with infants without acute phase response. Hence, using indicators of micronutrient status without considering the effects of the acute phase response results in a distorted estimate of micronutrient deficiencies, whose extent depends on the prevalence of infection in the population.
In this study the effects of supplementation of iron and zinc, alone or combined, on iron status, zinc status and growth in Indonesian infants is investigated. Micronutrient deficiencies are prevalent in infants in developing countries, and deficiencies often coexist; thus, combined supplementation is an attractive strategy. However, little is known about interactions between micronutrients. In a randomized, double-blind, placebo-controlled supplementation trial, 478 infants, 4 mo of age, were supplemented for 6 mo with iron (10 mg/d), zinc (10 mg/d), iron + zinc (10 mg of each/d) or placebo. Anthropometry was assessed monthly, and micronutrient status was assessed at the end of supplementation. Supplementation significantly reduced the prevalence of anemia, iron deficiency anemia and zinc deficiency. Iron supplementation did not negatively affect plasma zinc concentrations, and zinc supplementation did not increase the prevalence of anemia or iron deficiency anemia. However, iron supplementation combined with zinc was less effective than iron supplementation alone in reducing the prevalence of anemia (20% vs. 38% reduction) and in increasing hemoglobin and plasma ferritin concentrations. There were no differences among the groups in growth. The growth of all groups was insufficient to maintain the same Z-scores for height for age and weight for height. There is a high prevalence of deficiencies of iron and zinc in these infants, which can be overcome safely and effectively by supplementation of iron and zinc combined. However, overcoming these deficiencies is not sufficient to improve growth performance in these infants.
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