Trial on timing of introduction to solids and food type on infant growth.

OBJECTIVE: The optimal time and choice of solid foods to introduce to an infant's diet is unknown. The aim of this randomized trial was to determine whether early versus late introduction of solid foods and commercially prepared versus parent's choice of solid foods affects growth or body composition in the first year. METHODS: White infants (n = 165) were recruited before 3 months of age and were randomized to receive: 1) commercially prepared solid foods (commercial) from 3 to 12 months, 2) commercially prepared solid foods from 6 to 12 months, 3) parent's choice of solid foods (choice) from 3 to 12 months, or 4) parent's choice of solid foods from 6 to 12 months. Anthropometrics and body composition, using dual energy x-ray absorptiometry, were determined at 3, 6, and 12 months. Three-day diet diaries were completed at 3, 6, 9, and 12 months. RESULTS: There were no differences in growth or body composition between infants in early versus late introduction groups or commercial versus choice groups at any age. The total energy intake was not different among infants in the early compared with the late group at any age. Infants in the commercial group consumed less protein calories at 9 months (80 +/- 3 kcal/d vs 88 +/- 3 kcal/d) and 12 months 101 +/- 5 kcal/d vs 148 +/- 5 kcal/d), less fat calories at 12 months (263 +/- 10 kcal/d vs 343 +/- 10 kcal/d), and less total calories at 12 months (884 +/- 24 kcal/d vs 1022 +/- 25 kcal/d) compared with the choice group. CONCLUSION: The early introduction of solid foods to an infant's diet does not alter growth or body composition during the first year of life and results in a displacement of energy intake from formula. Infants consuming commercially prepared foods have a decreased caloric intake from protein and fat; however, despite this difference, there is no effect on growth or body composition.

Effectiveness of iron-fortified infant cereal in prevention of iron deficiency anemia.

BACKGROUND: Iron deficiency continues to be a common problem among infants throughout the world. Iron-fortified formula is effective in preventing iron deficiency but the benefit of iron-fortified cereal is controversial. METHODS: We compared iron-fortified rice cereal to unfortified rice cereal in infants who were exclusively breast-fed for more than 4 months and to iron-fortified formula in infants who were weaned to formula before 4 months of age. The design was double blind in respect to the presence or absence of fortification iron in the cereal or formula and included 515 infants who were followed on the protocol from 4 to 15 months of age. Rice cereal was fortified with 55 mg of electrolytic iron per 100 g of dry cereal and infant formula with 12 mg of ferrous sulfate per 100 g of dry powder, levels approximating those in use in the United States. Measures of iron status were obtained at 8, 12, and 15 months. Infants with hemoglobin levels of < 105 g/L were excluded from the study and treated. RESULTS: Consumption of cereal reached plateaus at means of about 30 g/d after 6 months of age in the formula-fed groups and 26 g/d after 8 months in the breast-fed groups; these amounts are higher than the 19-g/d mean intake by the 73% of infants who consume such cereal in the United States. Among infants weaned to formula before 4 months, the cumulative percentages of infants excluded for anemia by 15 months were 8%, 24%, and 4%, respectively, in the fortified cereal, unfortified cereal and formula, and fortified formula groups (P < .01 unfortified vs either fortified group; the difference between the two fortified groups was not significant). In infants breast-fed for more than 4 months, the corresponding values were 13% and 27%, respectively, in the fortified and unfortified cereal groups (P < .05). Mean hemoglobin level and other iron status measures were in accord with these findings. CONCLUSION: Iron-fortified infant rice cereal can contribute substantially to preventing iron deficiency anemia.

Dietary guidelines for infants: a timely reminder.

The 1995 edition of Dietary Guidelines for Americans has recently been released. In anticipation of the heightened attention that these revised will undoubtedly receive, there is renewed discussion about the need for Dietary Guidelines for Infants. These guidelines would reinforce to parents and nutrition professionals that many diet strategies designed to promote adult health and nutrition are inappropriate for infants and children under the age of two. These guidelines, developed in 1994 by the Gerber Products Company, seek to distinguish the unique dietary needs of this vulnerable population.

Fatty acid patterns in iron-deficient maternal and neonatal rats.

To determine the effects of maternal iron deficiency on lipid composition and fatty acid patterns in offspring, rats were fed ad libitum diets containing 5 ppm iron (deficient) (n=8) or 320 ppm iron (control) (n=7) and deionized water from day-1 of gestation through day-18 of lactation. On day-2 of lactation, litters were standardized to three male and three female pups. On day-18, pups were fasted for 4 hr before tissue and blood collection. Significant changes in serum and liver lipid concentrations and fatty acid patterns were observed in deficient pups. Serum triglycerides, cholesterol and phospholipids and liver triglycerides, cholesterol, and cholesteryl esters were increased. In deficient pups, percentage total fatty acids of 14:0, 16:1, 18:1, 18:2 from serum lipids were increased; in liver, 14:0, 18:2, 18:3 were increased; 18:0 and 20:4 were decreased in both serum and liver. Dam serum lipid levels did not differ between groups. Lipid changes observed in iron-deficient pups did not consistently reflect the milk, serum or liver lipid patterns observed in dams. Altered lipid composition and fatty acid patterns of iron-deficient pups thus appear to be of endogenous origin.

Carnitine levels in iron-deficient rat pups.

Hypertriglyceridemia and fatty livers have been observed in pups of Fe-deficient rats. Lowered tissue carnitine level is proposed as a mechanism responsible for altered lipid metabolism. Two hydroxylases involved in carnitine synthesis have been shown to require Fe in vitro. To determine if dietary Fe deficiency reduces tissue carnitine levels, two groups of 12 rats were fed 6 ppm Fe (-Fe) or 250 ppm Fe (+Fe) ad libitum from d 1 gestation to d 16 lactation. Feeding -Fe diets to dams resulted in 15% lower hemoglobin levels in pups on d 2 (P less than 0.02) and 50% lower levels on d 16 (P less than 0.001). Total carnitine level (nanomoles/milligram noncollagen protein) and triacylglycerol were assayed in pup tissues on d 2 and 16. While tissue carnitine and triacyglycerol was similar on d 2, d 16 liver carnitine was lower (P less than 0.001), triacylglycerol was eightfold higher in -Fe pups than in controls. Fe deficiency did not alter either carnitine concentration in milk on d 2 or 16 or the concentration of amino acid precursors of carnitine in milk on d 16. Decreased carnitine levels in the -Fe rat pup are contribute to triacylglycerol accumulation in liver.

Impaired ketogenesis in iron-deficient rat pups.

Livers of Fe-deficient rat pups contain significantly less carnitine and more triacylglycerol (TG) than livers of control pups. Carnitine affects ketogenesis (KG), which is a vital adaptation in the neonate. To determine if KG is impaired by low carnitine in Fe-deficient pup liver, ketone body synthesis was measured in liver mitochondria from 15-d-old pups. Litters from Fe-deficient (-Fe) and Fe-adequate (+Fe) dams were orally supplemented with water (W) as a control, 18 mM ferrous sulfate, or 10 mM L-carnitine from d 8 through d 15 of lactation. The amount of ketone bodies (beta-hydroxybutyrate + acetoacetate) synthesized was 68% less (P less than 0.05) in -FeW pups than in +FeW pups. Iron or carnitine supplementation increased KG in -Fe pups to +Fe KG levels, but carnitine did not affect KG in +Fe pups. Liver TG in +Fe pups was not altered by supplementation, but liver TG was -FeW pups. The data support the hypothesis that in the Fe-deficient suckling rat -FeW pups. The data support the hypothesis that in the Fe-deficient suckling rat, low carnitine levels may contribute to impaired ketogenesis and increased lipids in liver.

Postweaning carnitine supplementation of iron-deficient rats.

Severe iron deficiency in the suckling and weanling rat is associated with lipid accumulation in serum and liver, impaired ketogenesis in the suckling pup and low levels of carnitine in some tissues. Carnitine has been effective in reducing high triacylglycerol levels in humans and rats. This study examined tissue triacylglycerol concentrations of iron-deficient rats supplemented with carnitine or iron. Iron-adequate (C) and iron-deficient (D) pups were weaned to diets containing 38 ppm Fe (c) or 6 ppm Fe (d) with or without 0.2% DL-carnitine (Carn) resulting in six experimental treatments: CcCarn, DdCarn, Cc, Cd, Dc, Dd. Males received the diets for 2 wk and female littermates for 4. After 2 and 4 wk, carnitine supplementation significantly increased carnitine content in liver, heart and skeletal muscle by 30-60% in rats from control and Fe-deficient dams. Carnitine treatment significantly lowered the triacylglycerol level in liver of 49-d-old Fe-deficient females, but did not affect other tissues at either time point compared to other dietary treatments. Fe supplementation did not increase carnitine content in tissues, but did reduce triacylglycerol levels in liver by 4 wk and in skeletal muscle at both time points. Possible mechanisms by which iron and carnitine may lower lipids are discussed.