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Infants fed a soy formula supplemented with selenite had plasma and erythrocyte selenium values lower than those of infants fed human milk. However, plasma and erythrocyte glutathione peroxidase activities were normal, indicating that the physiologic requirement for selenium was being met.
Anthropometric indexes from 1 to 24 mo were compared between matched cohorts of infants either breast-fed (BF, n = 46) or formula-fed (FF, n = 41) until > or = 12 mo. Neither group received solid foods before 4 mo. Weight-for-length was significantly greater among FF infants from 7 to 24 mo. In both groups, skinfold thickness (triceps, biceps, subscapular, flank, and quadriceps) and estimated percent body fat (%FAT) increased rapidly during the first 6-8 mo and declined thereafter. At all sites except biceps, FF infants had larger skinfold thicknesses in later infancy (particularly 9-15 mo) than did BF infants; %FAT was significantly higher from 5 to 24 mo. Lower energy intake among BF infants explained the difference between groups. Maternal and infant fatness were positively correlated at 12-24 mo. Breast-milk lipid and energy concentration were unrelated to infant fatness. These results indicate that infants BF for > or = 12 mo are leaner than their FF counterparts.
Malondialdehyde (MDA) levels in infant milk formulas have been monitored by using an aqueous acid extraction method combined with the thiobarbituric acid method (TBA-test). Vegetable oils, with a remarkable content of polyunsaturated fatty acids (PUFA) are used to enrich the infant milk formulas. As PUFA are more susceptible to autoxidation, it becomes of great interest to have information about the safety and preservation of these products. We monitored MDA content in twenty of the most popular infant milk formulas and in some commercial cow milk samples and compared the obtained data. Levels of MDA ranged between 200 and 1200 ppb: all values but one were higher, up to five times, than those found in cow milk samples. To evaluate the accuracy of the data obtained from the TBA-test, some samples were also analyzed with an HPLC derivative method: preliminary results show a good agreement between the two analytical techniques.
Infants (n = 52) allergic to cow's milk protein and extensively hydrolyzed formulas received an amino acid-based formula. The amino acid-based formula proved to be safe, with infants exhibiting an overall gain in length and weight. Children with allergy restricted to extensively hydrolyzed formulas were diagnosed earlier and tolerated cow's milk protein earlier than children with multiple food allergy.
OBJECTIVE: To determine if docosahexaenoic acid (DHA) and arachidonic acid (ARA) supplementation influences growth or visual acuity of formula-fed premature infants. STUDY DESIGN: Double-blind, multi-center study of 194 premature infants given preterm formula with no DHA or ARA (control), 0.15% energy DHA, or 0.14% DHA + 0.27% ARA from single-cell triglycerides for at least 28 days and then fed term formula (no DHA or ARA) to 57 weeks postmenstrual age (PMA), with 90 breast-fed term infants as reference. RESULTS: Infants fed DHA+ARA formula gained weight significantly faster (post-hoc analysis) during preterm formula feeding than control infants (34.7 vs. 30.7 g/d) and had weights and weight:length ratios not different from term breast-fed infants at 48 and 57 weeks PMA. Infants fed control or DHA formula had lower body weights than term infants. Red blood cell phosphatidylethanolamine ARA was significantly correlated to weight gain during preterm formula feeding and to weight and length at 40, 48, and 57 weeks PMA (r = 0.19 to 0.24, P =.004-.02). Providing DHA or DHA+ARA during the preterm period had no effect on subsequent visual acuity or incidence of adverse events. CONCLUSIONS: Feeding DHA+ARA from single-cell triglycerides enhances weight gain in formula-fed premature infants with no evidence of adverse effects.
Thirty-four premature infants weighing less than 1500 grams at birth were fed preterm formula (formula), preterm infant formula manufactured to contain a balance of C20 and C22 omega 6 and omega 3 fatty acids within the range characteristic of human milk (LCPE-formula) or their mothers' expressed breast milk (EBM). Blood samples were obtained during the first week of life and after 28 days of feeding to determine the effect of feeding C20 and C22 omega 6 and omega 3 fatty acids on plasma lipids. Fatty acid analyses of red blood cell phospholipids indicated few differences between dietary treatment and age. Fatty acid content of plasma cholesterol esters indicated a high plasma cholesterol linoleate level for infants fed formula and a reduced content of C20 and C22 omega 6 and omega 3 fatty acids. For infants fed the modified formula (LCPE-formula) the levels of 20:4 omega 6, 20:5 omega 3 and 22:6 omega 3 were higher than observed for the formula group and similar to those observed for infants fed EBM. By the fifth week of life, feeding the modified formula resulted in plasma phospholipid levels of C20 and C22 omega 6 and omega 3 fatty acids similar to levels of C20 and C22 omega 6 and omega 3 fatty acids found in infants fed EBM and significantly higher than levels characteristic of infants fed formula. It is concluded that infants fed LCPE-formula illustrate an overall balance between C20 and C22 omega 6 to omega 3 fatty acids in the plasma similar to that characteristic of infants fed human milk.
Breast-fed and formula-fed infants (n = 65) were studied at 1 and 4 mo of age to elucidate differences in energy utilization between feeding groups. Gross energy intake at 1 mo was comparable between groups but was statistically different at 4 mo. Weight, length, and weight gain were not different between groups. Energy expenditure 0-4 h postprandially did not differ between feeding groups. Sleeping metabolic rates (SMRs) were not different but minimal observable energy expenditures standardized by weight were lower among 4-mo-old breast-fed infants (p less than 0.03). No differences were found between feeding groups in thermic effect of feeding (TEF). Activity patterns revealed that breast-fed infants slept less than formula-fed infants (p less than 0.04). Disparities in energy intake observed between breast-fed and formula-fed infants at 4 mo of age did not result in statistically significant differences in growth rate, SMR, or TEF.
Aluminum (Al) impairment of bone matrix formation and mineralization may be mediated by its direct effect on bone cells or indirectly by its effect on parathyroid hormone and calcium metabolism. Its toxic effects are proportional to tissue Al load. Al contamination of nutrients depends on the amount of Al present naturally in chemicals or from the manufacturing process. Intravenous calcium, phosphorus, and albumin solutions have high Al (greater than 500 micrograms/L), whereas crystalline amino acid, sterile water, and dextrose water have low Al (less than 50 micrograms/L) content. Enteral nutrients including human and whole cow milk have low Al, whereas highly processed infant formulas with multiple additives, such as soy formula, preterm infant formula, and formulas for specific disorders are heavily contaminated with Al. Healthy adults are in zero balance for Al. The gastrointestinal tract excludes greater than 95% of dietary Al, and kidney is the dominant organ for Al excretion. However, even with normal renal function, only 30-60% of an Al load from parenteral nutrition is excreted in the urine, resulting in tissue accumulation of Al. The risk for Al toxicity is greatest in infants with chronic renal insufficiency, recipients of long term parenteral nutrition, i.e., no gut barrier to Al loading, and preterm infants with low Al binding capacity. The rapid growth of the infant would theoretically potentiate Al toxicity in all infants, although the critical level of Al loading causing bone disorders is not known. To minimize tissue burden, Al content of infant nutrients should be similar to "background" levels, i.e., similar to whole milk (less than 50 micrograms/L).
The levels of individual proteins and other nitrogen containing substances differ considerably between cow's milk and human milk. Therefore, during manufacture of infant formulas, attempts are made to simulate the protein composition of human milk. However, the composition and nutritional characteristics of human milk protein are incompletely known. In this paper, the protein quality of breast milk protein with and without the non-protein-nitrogen (NPN) substances present in human milk was studied with growing rats and compared to two formulas, one "adapted" commercial infant formula and a suggested further modified, possibly improved, infant formula. Detailed examinations of protein and amino acid composition of the test diets are given. Breast milk protein with added NPN substances showed a lower protein quality than all other test proteins. Breast milk protein without NPN substances and the protein of the suggested infant formula were of similar quality while the protein of the commercial adapted formula was significantly better than all other test proteins. The use of rat growth assays in the evaluation of protein quality of infant formulas is discussed.
We conducted a randomized double-blind trial of a cow's milk infant formula with increased iron fortification in order to confirm its safety and to measure its effects on iron status and immune function. A group of full-term, well nourished and healthy infants was followed from the age of 3 months to 1 year. A control group of 74 infants was given a commercially available infant formula containing 8.3 mg Fe/100g. The test group of 75 infants received a similar formula with 40 mg Fe/100 g. The formula with the extra iron proved to be safe and, when compared with the control group, the children in the test group had significantly improved iron status as reflected by the proportion of children classed as normal (25 of 61 cf. 44 of 65; p less than 0.003), and by the mean values of the haemoglobin concentration (11.5 cf. 11.9 g/dl; p = 0.04), red cell distribution width (15.5% cf. 14.4%; p = 0.0005), red cell zinc protoporphyrin (3.4 cf. 4.0 micrograms/g Hb; p = 0.04) and ferritin (29 cf. 17.3 micrograms/l; p = 0.004). The extra iron fortification depressed zinc concentration in plasma (90.6 cf. 83.5 micrograms/l; p = 0.05). There was no significant difference between the two groups for laboratory measures of immune function or for incidence of infection. No adverse effects such as infection could be attributed to the increased iron. We conclude that iron fortification of cow's milk infant formula may be safely increased to 40 mg/100 g (i.e. by a factor of 4.8 over the common concentration of 8.3 mg/100 g), but that this has less than the expected effect on iron status. Further studies are required to define (a) the long-term role of facilitators of iron absorption such as ascorbic acid, (b) the interaction of iron with absorption of divalent trace elements such as zinc, and (c) the effect of iron status on immune function and susceptibility to infection.
A spectrophotometric method based on the reaction between available lysine and ortho-phthaldialdehyde (OPA) was adapted and validated for fluorometric determination of the chemically available lysine contents in milk matrices (UHT and conventional in-bottle sterilized cow milk, milk-based infant formulas and infant formula ingredients). The values of the analytical parameters show its usefulness as a routine method (linearity, r = 0.9992; detection limit, 0.0066 mg/mL assay; accuracy, 99-108%; precision, intra-day 2.1-5.9% and inter-day 3.5 10.2%). No statistically significant differences (p < 0.05) were found between the values obtained with the adapted method and those obtained applying the 1-fluoro-2,4-dinitrobenzene (FDNB) (Carpenter) technique. The OPA method was used to measure the chemically available lysine contents in UHT and sterilized milk marketed in Spain, to study the evolution of chemically available lysine during the shelf-life of UHT milks, and finally the quality of name- and store-brand UHT milks was also compared. No statistically significant differences (p < 0.05) were found between either the available lysine contents of the same type of UHT or sterilized milk or between store- and name-brand UHT milks. Statistically significant differences (p < 0.05) were found between the chemically available lysine contents in UHT and sterilized milk. Losses of chemically available lysine ranging from 2.7 to 29% were obtained during the shelf-life of UHT milk.
We tested the hypothesis that amino acid intake from infant formulas modified to be similar to human milk would result in indices of protein metabolism more like those in human milk-fed infants. Formula-fed infants received for 12 weeks one of three isocaloric formulations of a whey-adapted formula that differed in protein concentration: 11, 13, or 15 g/L. Infants consumed similar volumes of formula or human milk. Serum urea nitrogen concentrations reflected the protein content of the diets. Plasma indices of protein nutritional status were normal and did not differ among groups. Growth rates of all infants were normal and similar. Serum indicators of protein nutritional status varied with age, which made comparisons of formula-fed infants with human milk-fed infants difficult. Plasma concentrations of leucine and isoleucine at 4 weeks of age were higher in infants fed the formula containing 15 g protein/L when compared with those of infants fed the other two formulas or human milk. At 8 and 12 weeks of age, all formula-fed infants had plasma amino acid profiles that did not differ significantly from each other except for isoleucine, which was lower in the 11-g/L group. We found that providing formulas with an amino acid pattern similar to that of human milk did not produce a plasma amino acid pattern identical to that of the breast-fed infant. This observation suggests that other factors, such as the hormonal response to feeding, differing nutritional bioavailability of amino acids from human and bovine milk proteins, and the changing quantity and type of amino acids with advancing lactation, influence plasma amino acid concentrations.
The first months of life represent a critical period for the maturation of the infant's immune system and, thus, a window of opportunity for measures to reduce the risk of disease. We hypothesized that specific probiotics might promote mucosal immunologic maturation in formula-fed infants. The numbers of cow's milk-specific and total IgA-secreting cells were measured at 3, 7, and 12 mo of age in a double-blind placebo-controlled study of 72 infants with early artificial feeding. The infants consumed infant formula supplemented with specific probiotics (Lactobacillus GG and Bifidobacterium lactis Bb-12) or placebo during the first year of life. Further analyses of the serum concentrations of the IgA-inducing cytokine TGF-beta2 and the soluble innate microbial receptor sCD14 were conducted. The numbers of cow's milk-specific IgA secreting cells were significantly higher in infants receiving probiotics compared with those receiving placebo (p = 0.045, ANOVA for repeated measures). At 12 mo of age, the serum concentrations of sCD14 were 1479 pg/mL [95% confidence interval (CI) 1373-1592] in infants receiving probiotics and 1291 pg/mL (95% CI 1152-1445) in infants receiving placebo (p = 0.046). Administration of the probiotics Lactobacillus GG and Bifidobacterium lactis Bb-12 at the time of introduction of cow's milk in the infant's diet results in cow's milk-specific IgA antibody responsiveness that may be the result of increased production of sCD14.
Adherence of medium-chain triglyceride (MCT) oil to feeding tubes during gavage feeding of Enfamil formula was quantitated. Infants were fed similar volumes of either unfortified formula (n = 11) or MCT oil-fortified formula (0.5 ml/oz); either the MCT oil was mixed with the formula before feeding (n = 11) or the MCT oil was delivered into the feeding tube and then was followed by formula (n = 11). The fat residue in the feeding sets was quantitated by gravimetry, and individual fatty acids were characterized by gas-liquid chromatography. The data show that only trace amounts of lipid (0.23 +/- 0.04%) adhered to feeding sets during feeding of unfortified formula. Significantly more lipid (p less than 0.0005) adhered when formula was fortified with MCT oil, and the method of feeding greatly affected lipid adherence, i.e., 1.52 +/- 0.21% when the MCT oil was followed by formula versus 10.20 +/- 1.76% when the MCT oil was mixed with formula before feeding. Analysis of the fat residue of fortified formula showed that greater than 90% was composed of C8:0 and C10:0, the major fatty acid components of MCT oil. We suggest that care be exercised when fortifying infant formula with MCT oil.
To assess toxicokinetics of polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs), oral intake and fecal excretion were measured in two breast-fed infants and one formula-fed infant during the 1st y of life. The intake of these compounds was up to 50 times higher in the breast-fed infants. In these children, fecal excretion of the main tetra- to hexachlorinated congeners was less than 9% of the intake at age of 1 and 5 mo, indicating almost complete intestinal absorption during breast-feeding. In contrast, distinctly higher fecal excretion rates were observed for the hepta- and octachlorinated compounds. Despite much lower PCDD/PCDF intake after weaning, concentrations in stool fat did not decrease substantially. We conclude that concentrations in fecal fat more or less reflect those in body fat. Additionally, PCDD/PCDF concentrations were measured in blood fat of all infants (and in a second formula-fed baby) at the age of 11 mo. International toxicity equivalent (I-TEq) concentrations in the formula-fed infants were less than 25% of maternal values and about 10 times lower than in the infants breast-fed for 6-7 mo. In the latter, a distinct accumulation was found for the tetra- to hexachlorinated congeners compared with maternal concentrations. We conclude that accumulation of PCDDs and PCDFs in infants is as high as expected on the basis of intake data and assuming complete absorption and negligible elimination during the 1st y of life.
7-Ketocholesterol and 7-ketositosterol were chosen as reliable markers of the oxidation of cholesterol and phytosterols in infant milk formulas and infant milk cereals. A reversed-phase HPLC method was developed to measure them simultaneously in infant formulas. This method was then tested on a wide range of infant milk formulas and milk cereals on sale in Italy whose lipid composition is representative of the most common commercial formulas. The analytical results revealed no significant differences in the extent of oxidation of cholesterol and sitosterol. As the level of 7-ketocholesterol often followed the cholesterol level, a cholesterol content similar to that of human milk produced amounts of cholesterol oxides with possible negative effects on infant health. In contrast, the low cholesterol content of milk cereals never produced amounts of cholesterol oxides high enough to cause concern. The contents of phytosterols and hence their oxides were always low.
One hundred reconstituted milk-based infant formulae (IMF) representative of 10 leading brands available in many European Economic Community countries were examined for Bacillus cereus and for the presence of diarrheal enterotoxin. Sixty-three reconstituted IMF supported growth of the organism after 14 h at 25 degrees C, and in 4 of these, which contained maltodextrin, enterotoxin was detected. Reconstituted IMF (and basal synthetic media) supplemented with > or = 0.1% maltodextrin supported both growth of B. cereus and diarrheal toxin production when incubated for 14 h or more at 25 degrees C.
As an index of iron absorption, erythrocyte incorporation of the stable isotope, 58Fe, was determined 14 and 42 d after the administration of 58Fe-labeled ferrous sulfate to 56-d-old exclusively breast-fed infants and to infants fed a low-iron (1.8 mg/L) formula. Each infant received a dose of 0.6 to 1.0 mg of iron with ascorbic acid between feedings on each of 3 consecutive d. Fourteen d after administration of the 58Fe-labeled iron doses (age 70 d), arithmetic mean incorporation of the 58Fe label into erythrocytes by breast-fed infants was 20.0% of the dose--only slightly less than that reported for erythrocyte incorporation of iron by fasting adults fed small quantities of 59Fe-labeled human milk. Erythrocyte incorporation of iron by the formula-fed infants was 6.9% of the dose, suggesting that, even between feedings, components of infant formula exerted a major inhibitory effect on iron absorption. For reasons that are not clear, the percentage of the administered label incorporated into erythrocytes was significantly greater in breast-fed (but not in formula-fed infants) at 112 d of age than at 70 d of age.