Levels of aluminium in infant formulae.
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The effect of varying concentrations of ascorbic acid on the absorption of iron from a soy-based infant milk formula containing 6 mg iron/100 g was examined in 64 adult Indian females using the extrinsic radioactive tag method. The corrected geometric mean absorption from the basic soy formula was only 1.8%. Addition of ascorbic acid in a concentration of 40 mg/100 g, did not significantly increase absorption (3.3%; t = 1.8, p greater than 0.07) but raising the concentration to 80 mg/100 g did so (6.9%; t = 2.4, p less than 0.02). No further significant increase was noted when the concentration of ascorbic acid was increased to 160 mg/100 g (7.7%; t = 0.4, p greater than 0.7). The inhibitory effect of soy on iron absorption was further demonstrated by a direct comparison between the soy-based formula and a similar product based on cows' milk. The comparison was made at two concentrations of ascorbic acid. At 40 mg/100 g the geometric mean iron absorption from the soy formula was 2.4% compared with 5.3% from the milk formula (t = 2.8, p less than 0.02), while the corresponding values at 80 mg ascorbic acid/100 g were 7.2 and 19.5%, respectively (t = 3.4, p less than 0.02). The present results confirm the marked inhibitory effect of soy protein on iron absorption and calculations from the absorption figures suggest that such formulas should contain at least 12 mg/100 g iron together with ascorbic acid in a molar ratio of approximately 4:1 if they are to be adequate in terms of iron nutrition.
Cows' milk--fresh, boiled, and processed in different ways for the domestic market, and various infant milk formulae--was investigated for its sensitising capacity in the guinea-pig after being fed for 37 days. The anaphylactic sensitising capacity was considerably reduced by heat-treatment. As heat becomes more intense and more prolonged so beta-lactoglobulin and casein become less sensitising. It should be stressed that these were results from experiments on guinea-pigs drinking milk. Should they be found to apply to the human infant too, it seems that it would not be impossible to manufacture a non-sensitising but fully nutritive milk product. The sensitising capacity of fresh and boiled goats' milk was examined too, and it was found that boiling reduced the sensitising capacity to an even greater extent than was the case with cows' milk.
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The osmolalities of breast milk and of 36 products that may be fed to infants were determined by the freezing-point depression method. A wide range of osmolality was observed among formulas that provide 67 kcal/100 ml, and many have osmolalities greater than 400 mOsm/kg of water. Reconstituted powdered formulas have osmolalities that are widely varied from batch to batch, are greater when prepared by scoop measures when the osmolalities of corresponding ready-to-feed formulas, and are greater than the osmolalities of the formulas prepared by weighed measures from the manufacturer's formulation. The osmolality of products for oral consumption should be considered in the selection of formulas for preterm infants.
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Human milk contains factors that protect suckling infants against enteropathogen-induced diarrhea. One nonspecific protective factor found in human milk is a small molecular weight material that protects suckling mice from death due to the heat-stable enterotoxin of Escherichia coli. This study demonstrated that cow's milk and most formulas derived from cow's milk also contain a factor(s) that can protect against heat-stable enterotoxin of E. coli in suckling mice.
About 50 metabolically important fatty acids can be identified in human milk. The extent of absorption of milk fatty acids varies considerably from infant to infant, particularly in pre-term infants, and requires more study. Human milk provides sufficient vitamins A and E for the term infant, but supplementation with vitamins D and K may be necessary. More research is needed on the amounts of the fat-soluble vitamins in human milk, the efficiency of transfer from mother to infant, the reasons for variation in different women, and the consequences to breast-fed infants of inadequate intake of vitamins D and K. Breast milk contains the PUFA needed by term infants who are able to synthesize the long-chain PUFA soon after birth. Pre-term infants fed formulae need supplementation with n3 and n6 long-chain PUFA, since formulas currently do not contain these acids. More work is needed to determine the requirements for n3 and n6 fatty acids, expressed as weights per kilogram. A larger data base using improved analytical procedures to study the nature and content of lipids in human milk is needed. The impact of maternal genetics and diet on fatty acids in milk should be studied, as well as the effect of maternal diet on eicosanoids secreted by the mammary gland. Information on the structure and function of the milk fat globule and its membrane is needed. Little is known about the effect of milk banking on milk lipids. The reader of this review will no doubt find other gaps in our knowledge of the lipid composition and nutritional value of milk that require additional investigation.
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OBJECTIVES: To come even closer to the functional composition of human milk, acidic oligosaccharides (AOS) from pectin were added to well known neutral prebiotics (galacto-oligosaccharides (GOS) and long-chain fructo-oligosaccharides (FOS)). The effect of AOS and GOS/FOS/AOS on intestinal flora, stool characteristics as well as acceptance and tolerance was investigated. METHODS: Human milk contains 75% to 85% neutral and 15% to 25% acidic oligosaccharides. In this prospective, randomized, double blind study, a mixture of 80% neutral oligosaccharides (from long-chain galacto- and long-chain fructo-oligosaccharides) with 20% acidic oligosaccharides derived from pectin hydrolysis was investigated. Forty-six term infants were fed a standard formula supplemented with either maltodextrin as control (n=15), or with 0.2 g acidic oligosaccharides (n=16), or with the latter plus 0.6 g neutral oligosaccharides (mixture of galacto- and fructo-oligosaccharides; n=15). Fecal flora using plating technique and pH were measured. Stool characteristics and possible side effects (crying, vomiting, and regurgitation) were recorded. RESULTS: There was no difference in the bifidobacteria counts between the control and the group supplemented with acidic oligosaccharides alone (8.75+/-0.50 vs. 8.58+/-0.94 log colony forming units [CFU]/g stool). In infants fed the combination of acidic and neutral oligosaccharides, bifidobacteria were increased (9.61+/-0.70 log CFU/g stool; P<0.01). The same pattern was observed with lactobacilli. Stool consistency was softest in infants fed the complete oligosaccharide mixture, but also in those fed formula supplemented with acidic oligosaccharides alone, the stool consistency was significantly softer compared with the control group. Fecal pH increased in the controls, remained constant in acidic oligosaccharides alone, and decreased in the complete mixture of oligosaccharides group. CONCLUSION: There was no difference in growth, crying, vomiting, and regurgitation patterns between the groups. In summary, acidic oligosaccharides from pectin hydrolysate are well tolerated as ingredient in infant formulae but do not affect intestinal microecology.
Aluminium toxicity occurred in two infants with congenital uraemia who had never received phosphate binders or other aluminium-containing agents or intravenous fluids. One patient was treated by peritoneal dialysis from the age of two weeks and died at three months after the sudden onset of neurological symptoms; the other died after one month of conservative management without dialysis. Brain aluminium concentration was high in both infants (6.4 and 47 micrograms/g, respectively) whereas bone aluminium content was normal and there were no histological changes or stainable aluminium on bone biopsy specimens. Both infants were fed with 'Similac PM 60/40'. To investigate possible sources of aluminium, powdered milk formula, sterilised water used for preparation of the feed, and dialysate concentrate (first patient) were analysed. Aluminium concentration was high (232 +/- 60 ng/ml) in powdered milk but negligible in sterilised water and dialysate concentrate (4 ng/ml and 3.4 +/- 2.4 ng/ml, respectively). These findings indicate that proprietary infant milk formula is another source of aluminium. Aluminium-free milk should contribute to the prevention of aluminium toxicity in infants with renal failure.
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OBJECTIVE: To investigate the effects of a milk formula supplemented with a alpha-linolenic acid (ALA) (18:2 n-6/18:3 n-3 ratio near 6/1) on plasma and red blood cell (RBC) fatty acids (FAs) in premature infants and compare with a non supplemented formula (18:2 n-6/18:3 n-3 = 22/1). DESIGN AND SUBJECTS: Infants of mothers who elected not to breast-feed were randomly assigned to either a high alpha linolenic formula (HLF: n = 31) group or a low alpha-linolenic formula (LLF: n = 32) control group. Infants fed human milk (HM: n = 25) were enrolled concurrently as a reference group. Anthropometric and biological measurements were made after two days (D2) and 15 d (D15) of enteral feeding and at the 37th week (W37) of postconceptual age. In HLF, the 18:3 n-3 content was 1.95% of total FAs (0.77% of total energy) and the 18:2 n-6/18:3 n-3 ratio was near 6/1. In LLF, the 18:3 n-3 content was 0.55% of total FAs (0.22% of total energy) and the 18:2 n-6/18:3 n-3 ratio was 22/1. RESULTS: ALA supplementation had minimal effect on the n-6 series, did not alter the anthropometric data and confirmed the conversion of ALA into docosahexaenoic acid (DHA). Throughout the study, it maintained, the RBC membrane DHA values within the confidence interval of those obtained in the HM group. Such was not the case with LLF CONCLUSION: alpha-linolenic acid supplementation (from Rapeseed oil and in a 18:2 n-6/18:3 n-3 ratio = 6) in premature infant formula can contribute efficiently to the maintenance of the n-3 status in the premature newborns.