One hundred four infants were randomly assigned to receive whole cow milk plus iron-fortified cereal (WCM + C) in accord with the previous recommendations of the Committee of Nutrition/American Academy of Pediatrics (CON/AAP); one of two iron-fortified, follow-up formulas; or an iron-fortified infant formula. Mean iron intakes and vitamin C exceeded the recommended dietary allowance in all groups. By 12 mo of age, mean ferritin and mean corpuscular volume were lower in the WCM + C group and significantly more infants had serum ferritin concentrations < 12 micrograms/L. We conclude that infants 6-12 mo of age fed whole cow milk and iron-containing table food are at risk of developing depleted iron stores but not anemia. The iron insufficiency in these infants is not due to inadequate intake of iron or vitamin C, but probably to relatively poor bioavailability of iron in infant cereal.

Abnormal growth is a common feature of thalassaemia major in children. In an attempt to determine whether it has a nutritional cause, 12 children aged 1 to 3 years with thalassaemia major were studied under metabolic ward conditions. Nutritional status was assessed by anthropometry and biochemistry before and after an intensive nutrition regimen. Five children had wasting or stunting on admission. As a result of the nutrition intervention, mean weight for height improved significantly. The mean height increase of0 4 cm after one month was not significant. Plasma zinc, depressed in half the children on admission, improved, as did (x tocopherol, while copper decreased. Plasma insulin-like growth factor-I also increased commensurate with improved growth. Fat absorption was normal in all children. Undernutrition is an important cause of associated growth disturbances in children with thalassaemia major. Malnutrition was primarily caused by inadequate nutrient intake, as indicated by the capacity to gain weight appropriately when provided with nutrition support, and by the absence of intestinal malabsorption. While long term studies are required to determine if nutritional support will prevent stunting, these results underscore its central role in preventing nutritional deficiencies and in promoting normal growth in thalassaemic children.

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Twelve thalassaemic children under 3 years of age received intensive nutritional support for one month and were discharged on a prescribed diet of locally available foods. Anthropometry, bioelectrical impedance analysis and dietary intake were longitudinally assessed. Mean energy intake was 20% greater than the recommended daily allowance during nutritional supplementation as compared with below the recommended daily allowance before and after the period of nutritional support. Weight, but not height, significantly increased during the support period and was due to increases in both fat free mass and fat mass. Body weight, fat free mass and fat mass declined in line with the reduced intake upon return home; however, height velocity accelerated and exceeded normal through the fourth month before resuming a below normal rate. It can be concluded that (1) nutritional stunting as the result of reduced nutrient intake is an important cause of growth failure in young children with thalassaemia and is responsive to nutritional support, (2) the deficit in height velocity was due to retarded truncal height growth, and (3) the bioelectrical impedance analysis method is suitable for body composition analysis of thalassaemic children. (Arch Dis Child 1997;76:509-512)