Nutritional support and growth in thalassaemia major.

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.

Nutritional factors and thalassaemia major.

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 of 0.4 cm after one month was not significant. Plasma zinc, depressed in half the children on admission, improved, as did alpha 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.

Effect of dietary fat on cardiovascular risk factors in infancy.

OBJECTIVE: To determine the effects of feeding regimens of varying fat composition on dietary intake and serum lipid and lipoprotein concentrations in older infants. DESIGN, SETTING, AND PARTICIPANTS: One hundred four healthy infants aged 4 to 6 months were enrolled from private pediatric practices or public health clinics and were randomly assigned to one of four feeding groups until 12 months of age. INTERVENTIONS: Infants received whole cow milk or a standard infant formula (48% to 49% of energy as fat from butterfat or a soy-coconut oil blend, respectively) or one of two nearly identical investigational lower fat follow-up formulas (36% kcal from a fat blend of palm olein, corn, and safflower oils) as their primary food source in addition to table foods. MAIN OUTCOME MEASURES: Nutrient intakes during the study period were characterized qualitatively and quantitatively. Serum lipids, lipoprotein concentrations, and anthropometrics were determined at baseline and at 12 months of age (study completion). RESULTS: Total energy intake was equivalent among feeding groups. Infants fed cow milk had higher mean daily intakes of total fat, saturated fat, monounsaturated fat, and cholesterol. Linoleic acid intake by infants fed cow milk, including that from table foods, was insufficient to meet current recommendations. Mean serum total cholesterol was significantly higher in the infants fed cow milk at age 12 months, whereas mean low density lipoprotein and apolipoprotein B were lower in the infants fed the follow-up formulas. Infants consuming the infant formula or whole cow milk demonstrated greater increases in mean serum total cholesterol, low density lipoprotein, and apolipoprotein B by 12 months of age compared with infants ingesting follow-up formula. Ponderal, linear, and head circumference growth was equivalent among feeding groups. CONCLUSIONS: (1) Older infants fed lower fat formula have adequate total energy intake and normal growth. (2) The fat composition of the diets fed to the infants influenced serum lipid and lipoprotein profiles. (3) The fat composition of cow milk is inferior compared with commercial formulas. (4) The optimal fat blend for older infants including the consequences of the standard practice of adding high percentage of coconut oil to infant formulas should be defined further.

Iron status and intake of older infants fed formula vs cow milk with cereal.

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.

Gastrointestinal blood loss in older infants: impact of cow milk versus formula.

Concerns that consumption of whole cow milk (WCM) by older infants may result in excessive gastrointestinal blood loss and subsequent iron deficiency led us to perform a prospective, randomized study in 104 infants. Infants were assigned to receive WCM beginning at 6 months or one of three formulas beginning at 4-6 months of age and followed until 12 months of age. Gastrointestinal blood loss was similar for all groups, as determined by both qualitative (Hemoccult II) and quantitative testing (HemoQuant). There was no association between concentration of fecal hemoglobin and volume of WCM consumed or iron status by 12 months of age. Of eight infants (seven WCM, one formula) who became iron-depleted, none had excessive fecal hemoglobin excretion. When pooled and analyzed regardless of feeding group, fecal hemoglobin increased with age and was greater at 11 and 12 months than at younger ages. We conclude that although infants fed WCM are at increased risk of developing iron depletion, the iron insufficiency is not due to gastrointestinal blood loss. We further conclude, based on our sample of normal infants age 4-12 months, that fecal hemoglobin concentrations of 0.5-0.8 mg/g stool correspond to the upper limits of normal, values much lower than in adults.