Fat intake and metabolism in Swedish and Italian infants

The purpose of the study was to compare fat intake and metabolism between two infant populations from Sweden and Italy given breast milk or similar infant formulas, but different weaning foods. Nutrient intake and fat metabolism were studied prospectively from 3-12 mo in 68 Swedish and 46 Italian healthy infants, breastfed or given similar infant formulas in combination with Swedish or Mediterranean weaning foods. Although nutrient intake and fat metabolism were similar at 6 mo, fat intake was lower at 12 mo in the Italian than in the Swedish formula group (p < 0.001). At 6 and 12 mo, higher dietary ratios of monounsaturated to saturated fatty acids (p < 0.01 and p < 0.001, respectively), and monounsaturated to polyunsaturated fatty acids (p < 0.05, p < 0.001) were found in the Italian than in the Swedish formula group. Total cholesterol and apolipoprotein B were lower at 6 mo (p < 0.01) in Italian breastfed infants than in Swedish ones. Lower concentrations at 6 and 12 mo of total cholesterol (p < 0.05, p < 0.05, respectively), apolipoprotein B (p < 0.05, p < 0.01) and triglycerides (p < 0.001, p < 0.01), and of apolipoprotein A1 (p < 0.01) at 12 mo, were found in the Italian formula group than in the Swedish one. In conclusion, plasma total cholesterol, apolipoprotein B and triglycerides were found to be lower in Italian infants than in Swedish infants during the second half of infancy. These findings may partly result from differences in fat compositions between Swedish and Mediterranean weaning diets and in total fat intake in late infancy. Differences in duration of breastfeeding and possibly in breast milk composition may also have influenced our results.     

Protein intake and metabolism in formula-fed infants given Swedish or Italian weaning foods

The aim of the study was to compare protein intake and metabolism between infants from two countries given similar infant formulae but different weaning foods. Healthy Swedish and Italian infants were studied between 3 and 12 mo. Infants in both populations were assigned to 1 of 3 infant formulae, containing 13, 15 or 18/20 g l^-1 of protein, given in addition to Swedish or Italian weaning foods. Protein intake from weaning foods was higher in Italian than in Swedish infants at 6 and 12 mo, whereas protein intake from formula at 6 mo and from formula/milk at 12 mo was similar in both populations. Plasma isoleucine, leucine, lysine, histidine and valine at 6 mo were lower in Italian than in Swedish infants fed formula with 13 g l^-1 of protein. All essential plasma amino acids were similar in Italian and Swedish groups at 12 mo. Serum urea was similar at 6 mo in corresponding formula groups, but was higher at 12 mo in the Italian than in the Swedish formula group. Serum albumin and growth were normal in both populations throughout infancy. In conclusion, formula with protein content of 13 g l^-1 seems to provide sufficient protein intake when combined with Swedish or Italian weaning foods during the second half of infancy, as indicated by normal serum albumin and normal growth. However, the bioavailability of protein and amino acids from weaning foods, in addition to their protein content, should be considered, as indicated by some indices of protein metabolism in the Italian infants.     

Th1 and Th2 chemokines, vaccine-induced immunity, and allergic disease in infants after maternal ω-3 fatty acid supplementation during pregnancy and lactation

We investigated whether the previously reported preventive effect of maternal ω-3 fatty acid supplementation on IgE-associated allergic disease in infancy may be mediated by facilitating a balanced circulating Th2/Th1 chemokine profile in the infant. Vaccine-induced immune responses at 2 y of age were also evaluated. Pregnant women, at risk of having an allergic infant, were randomized to daily supplementation with 1.6 g eicosapentaenoic acid and 1.1 g docosahexaenoic acid or placebo from the 25th gestational week through 3.5 mo of breastfeeding. Infant plasma was analyzed for chemokines (cord blood, 3, 12, 24 mo) and anti-tetanus and anti-diphtheria IgG (24 mo). High Th2-associated CC-chemokine ligand 17 (CCL17) levels were associated with infant allergic disease (p < 0.05). In infants without, but not with, maternal history of allergy, the ω-3 supplementation was related to lower CCL17/CXC-chemokine ligand 11 (CXCL11) (Th2/Th1) ratios (p < 0.05). Furthermore, in nonallergic, but not in allergic infants, ω-3 supplementation was linked with higher Th1-associated CXCL11 levels (p < 0.05), as well as increased IgG titers to diphtheria (p = 0.01) and tetanus (p = 0.05) toxins. Thus, the prospect of balancing the infant immune system toward a less Th2-dominated response, by maternal ω-3 fatty acid supplementation, seems to be influenced by allergic status.     

Protein intake in early infancy: effects on plasma amino acid concentrations, insulin metabolism, and growth

The effects of different protein intakes on wt gain, insulin secretion, and plasma concentrations of amino acids have been evaluated in a prospective study involving 30 normal term infants. The infants were studied from 4.0 to 6.0 mo of age. Ten infants were breast-fed (BF), the others were randomly divided into two groups of 10 infants. One group was fed a formula containing 1.3 g protein/100 mL (F 1.3), the other a formula with 1.8 g protein/100 mL (F 1.8). The formulas were isocaloric (72 kcal/100 mL), and the fat concentrations were 3.5 g/100 mL (F 1.3) and 3.2 g/100 mL (F 1.8). All infants received the same supplementary foods. The urinary C-peptide excretion in the infants fed the F 1.8-formula was 4.4 +/- 2.1 nmol/mmol creatinine or 19.4 +/- 12.9 nmol/m2, significantly higher than that in the infants fed the F 1.3-formula (2.6 +/- 1.5 and 7.9 +/- 5.1) or the BF infants (1.7 +/- 1.4 and 6.3 +/- 6.0). Gain in wt was 18.0 +/- 4.3, 19.9 +/- 3.9, 22.8 +/- 1.6 g/kg/wk and corresponded to protein intakes of 1.3 +/- 0.2, 1.9 +/- 0.3, and 2.6 +/- 0.2 g/kg/d, in the BF, F 1.3, and F 1.8 groups, respectively. Gain in length was 6.7 +/- 1.8 (BF-group), 6.2 +/- 2.5 (F 1.3-group), and 7.6 +/- 2.2 (F 1.8-group) mm/m/wk. Wt gain correlated with urinary C-peptide excretion at 6.0 mo (r = 0.51, p less than 0.01) and with protein intake (r = 0.43, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Iron supplements reduce erythrocyte copper-zinc superoxide dismutase activity in term, breastfed infants

AIM: To investigate whether iron supplements compromise copper status in infants. METHODS: 214 healthy, term, breastfed Swedish and Honduran infants were randomized to (1) iron supplements (1 mg/kg/d) from 4-9 mo of age, (2) iron supplements from 6-9 mo, or (3) placebo. Blood samples were obtained at 4, 6, and 9 mo and analyzed for plasma copper (p-Cu) and, at 9 mo, for copper/zinc-dependent superoxide dismutase (CuZn-SOD) activity. RESULTS: P-Cu increased with infant age. At 9 mo, Honduran infants had significantly higher p-Cu (1.40+/-0.29 vs 1.09+/-0.22 mg/l, p<0.001) and CuZn-SOD activity (1.09+/-0.29 vs 0.93+/-0.21 U/mg Hb, p<0.001) than Swedish infants. Infants receiving iron supplements from 4-9 mo had significantly lower CuZn-SOD at 9 mo of age (0.95+/-0.27 vs 1.08+/-0.24 U/mg Hb, p=0.023) than those receiving placebo.CONCLUSION: There is a physiologic increase in p-Cu during the first 9 mo of life. Differences in copper status between Swedish and Honduran infants may be due to genetic or nutritional differences. Iron supplementation decreases CuZn-SOD activity, probably due to a negative effect on copper status. Possible clinical implications remain to be elucidated.     

The effect of fish oil supplementation on heart rate in healthy Danish infants

Polyunsaturated n-3 fatty acids (n-3PUFA) may improve brain development and prevent cardiovascular disease. Heart rhythm is autonomically controlled and among the affected cardiovascular risk markers in adults. The aim of the study was to examine whether fish oil supplementation in late infancy could modify heart rate (HR) and heart rate variability (HRV). In a 2 x 2-intervention, 83 healthy Danish infants were randomized to +/- fish oil (3.4 +/- 1.1 mL/d) and cow's milk or infant formula from 9 to 12 mo of age. In 57 infants, 0.5-h ECG recordings were successfully obtained before and after the intervention and erythrocyte fatty acid composition was determined in 30 of these. Fish oil supplementation raised erythrocyte n-3PUFA content (p < 0.001). No significant group differences were seen in HR or HRV. However, a fish-oil x gender interaction was observed on mean RR interval (p = 0.001) with a 6% longer mean RR interval in fish-oil-supplemented boys (p = 0.007). Irrespective of gender, there was a positive association between the 9- and 12-mo changes in RR interval and erythrocyte n-3PUFA (p < 0.001). In infants with confirmed changes in erythrocyte n-3PUFA, mean RR interval was found to be longer (p = 0.011) in the fish-oil-supplemented groups. The study suggests that fish oil may affect heart rhythm in infants similar to that observed in adults. This may imply low n-3PUFA-status in late infancy and n-3PUFA influence on CNS function.     

Milk from mothers of both premature and full-term infants provides better antioxidant protection than does infant formula

We hypothesized that premature (PT) infants' mother's milk may provide antioxidant advantages compared with milk from mothers of full-term (FT) infants, and human milk may provide antioxidant properties not seen in infant formulas. We designed three experiments to test these hypotheses. Experiment 1 assessed resistance to oxidative stress of human milk and formulas designed for FT and PT infants. Experiment 2 determined differences in resistance to oxidative stress between milk from mothers of FT and PT infants, including analysis of catalase activity. Experiment 3 examined factors in human milk that may account for increased resistance to oxidative stress. In experiment 1, we induced physiologic oxidative stress in human milk (n = 5) and formula (n = 2) and measured ascorbate radical using electron paramagnetic resonance. Results indicated the following: 1) during oxidative stress, ascorbate may be spared in human milk compared with formula; 2) ascorbate radical production is more intense in formula compared with human milk, with or without oxidative stress; and 3) oxygen consumption in human milk is less than that in formula, with or without oxidative stress. In experiment 2, milk samples were collected from mothers of PT (n = 28) and FT (n = 17) infants at wk 1, 2, and 12 of lactation. No differences in oxygen consumption after oxidative stress appeared between PT and FT milk. Catalase levels in human milk increased with time. In experiment 3, addition of catalase, superoxide dismutase, and glutathione peroxidase to formulas (n = 4) increased resistance to oxidative stress. Denaturing endogenous enzymes did not decrease the ability of human milk to resist oxidative stress. Ferrous sulfate plus vitamin C added to human milk and formulas fortified with iron increased oxidative stress. Addition of iron chelators to formula reduced oxidative stress. In conclusion, human milk has better antioxidant protection than do formulas, perhaps because of the higher iron content of formulas. Milk from mothers of PT and FT infants has equal resistance to oxidative stress.     

Iron balance and iron nutrition in infancy

At birth, the total body iron content is approximately 75 mg/kg, twice that of an adult man in relation to weight. During the first 6 mo of life, total iron body content increases slightly and exclusive breastfeeding is sufficient to maintain an optimal iron balance. Thereafter, iron body content substantially increases and the infant becomes critically dependent on dietary iron, provided by complementary foods. Numerous factors may contribute to nutritional iron deficiency in infancy, the most important being low body iron content at birth, blood loss, high postnatal growth rate, and a low amount and/or bioavailability of dietary iron. We have documented that the prevalence of iron deficiency declined in Italy as iron nutrition improved and that early feeding on fresh cow's milk is the single most important determinant of iron deficiency in infancy. Healthy full-term infants should maintain optimal iron balance by consuming a good diet, which can be summarized as follows: breastfeeding should be continued exclusively for at least 5 mo and then together with complementary foods containing highly bioavailable iron; infants who are not breastfed or are partially breastfed should receive an iron-fortified formula, containing between 4.0 and 8.0mg/L iron, from birth to 12 mo of age; fresh cow's milk should be avoided before 12 mo of age.     

Iron balance and iron nutrition in infancy

At birth, the total body iron content is approximately 75 mg/kg, twice that of an adult man in relation to weight. During the first 6 mo of life, total iron body content increases slightly and exclusive breastfeeding is sufficient to maintain an optimal iron balance. Thereafter, iron body content substantially increases and the infant becomes critically dependent on dietary iron, provided by complementary foods. Numerous factors may contribute to nutritional iron deficiency in infancy, the most important being low body iron content at birth, blood loss, high postnatal growth rate, and a low amount and/or bioavailability of dietary iron. We have documented that the prevalence of iron deficiency declined in Italy as iron nutrition improved and that early feeding on fresh cow's milk is the single most important determinant of iron deficiency in infancy. Healthy full-term infants should maintain optimal iron balance by consuming a good diet, which can be summarized as follows: breastfeeding should be continued exclusively for at least 5 mo and then together with complementary foods containing highly bioavailable iron; infants who are not breastfed or are partially breastfed should receive an iron-fortified formula, containing between 4.0 and 8.0 mg/L iron, from birth to 12 mo of age; fresh cow's milk should be avoided before 12 mo of age.     

Onset of significant GH dependence of serum IGF-I and IGF-binding protein 3 concentrations in early life.

Forty-eight normal full-term Chinese babies (25 boys and 23 girls) were followed up every 2 mo in the first year and every 3 mo during the second year of life for anthropometric measurements. Blood samples were taken at birth and at 6, 10, 12, and 18 mo after birth for serum GH-binding protein, IGF-I, and IGF-binding protein 3 analysis. Onset of the childhood phase of growth in the infants was determined from the growth data plotted on Infancy-Childhood-Puberty growth charts. The serum GH-binding protein concentrations were low in cord blood but rose significantly at 6 mo, with slower rises in late infancy and early childhood. However, a significant rise in serum IGF-I and IGF-binding protein 3 levels was only observed from 10 mo of life onward. The change in IGF-I between birth and 6 mo was significantly correlated with length gain (r(2) = 0.35, p < 0.05) and body mass index gain (r(2) = 0.41, p < 0.01) during the same period. The 34 infants with onset of childhood phase of growth between 6 and 10 mo had a higher mean serum IGF-I value at 10 mo (8.8 +/- 5.8 nM versus 4.9 +/- 3.1 nM; p < 0.05) and higher length velocity between 10 and 12 mo (16.3 +/- 4.7 cm/y versus 8.8 +/- 4.3 cm/y; p < 0.001) compared with the 14 infants with a later onset after 10 mo of age. A significant correlation between a change in serum IGF-I and IGF-binding protein 3 levels was observed during the three 6-mo periods between birth and 18 mo, but a significant correlation between a change in serum GH-binding protein and a change in serum IGF-I or IGF-binding protein 3 levels was only seen between 12 and 18 mo of age. The multiple regression analysis (r(2) = 0.43, p = 0.0002) revealed that the change in serum GH-binding protein and IGF-I concentrations between 6 and 12 mo of age and the age of onset of childhood phase of growth could explain 43% of the length gain between 6 and 12 mo of age in our babies. The results of our study support the hypothesis that the onset of the childhood phase of growth is associated with the onset of significant GH action on growth.     

Alpha-1-antitrypsin concentration in human milk

Alpha-1-antitrypsin concentration was analyzed by immunoelectrophoresis in samples of human colostrum (n = 3) and of mature milk from mothers between 2 to 52 wk postpartum (n = 39), one of whom was known to be PiMZ with a PiZZ infant. All milk samples tested contained alpha-1-antitrypsin. The three colostrum samples contained 140, 520, and 250 mg/liter. The mature milk of women who had been lactating less than 6 months had a higher concentration (7.2 +/- 3.6 mg/liter) (mean +/- SD) than in the women who had been lactating 6-12 months (4.8 +/- 1.8 mg/liter) (p less than 0.03). The milk of the woman of Pi type MZ had an alpha-1-antitrypsin concentration of 7.0 mg/liter at 7 wk postpartum and 4.1 mg/liter at 52 wk. It has been previously demonstrated that enhanced absorption of intact proteins occurs in early infancy. The presence of antiproteases in human milk provided during early infancy may serve to inhibit the absorption of intact proteases, limiting their entry into the portal circulation.     

Does early hospital discharge with home support of families with preterm infants affect breastfeeding success? A randomized trial

The aim of the present study was to determine if earlier discharge of preterm infants (<37 wk) from hospital is safe and if it affects breastfeeding rates. In a pilot observational study, premature infants received full oral (sucking) feeds for a mean (SD) 7.7 +/- 7.9 d before discharge. In the main study, 308 preterm infants were randomly assigned to either Early Discharge (148 infants) when fully orally fed but not yet gaining weight or Routine Discharge (160 infants) when fully orally fed and also gaining weight before discharge. A further 122 mothers declined randomization. The Early Discharge group was followed by Visiting Nurse Specialists who were available 24 h a day, while the Routine group was followed by the Home Care Nurses available on week days. There were no significant differences between the groups in birthweight or gestational age. The Early Discharge group were discharged 2.5 +/- 2 d after full oral feeding compared to 4.4 +/- 2.7 d for the Routine group (p < 0.001) and 6.1 +/- 5 d for those who declined. However, there was no significant difference between the Early and Routine groups for breastfeeding either at discharge (80 vs 83%), or 6 wk (55 vs 60%) or 6 mo after discharge (36 vs 36%), or for weight gain, or rates of re-hospitalization (8.8% vs 11.9% at 6 wk, p = 0.37). Conclusion: Early discharge from hospital once a preterm infant can take full oral feeds does not alter later breastfeeding rates when adequate visiting nursing support is available.     

Cholinergic and oxidative stress mechanisms in sudden infant death syndrome

Aim:  To determine whether biochemical parameters of cholinergic and oxidative stress function including red cell acetylcholinesterase (AChE), serum/plasma thyroglobulin, selenium, iron, ferritin, vitamins C, E, and A affect risk in apparent life-threatening event (ALTE), sudden infant death syndrome (SIDS), and sudden unexpected death in infancy (SUDI). To assess these biochemical parameters as a function of age; and for influence of pharmacology and epidemiology, including infant health, care, and feeding practices.
Methods:  A multicentre, case–control study with blood samples from 34 ALTE and 67 non-ALTE (control) infants matched for age, and 30 SIDS/SUDI and four non-SIDS/non-SUDI (post-mortem control) infants.
Results:  Levels/activity of the biochemical parameters were not significantly different in ALTE vs. control infants, with the exception of higher vitamin C levels in the ALTE group (p = 0.009). In ALTE and control groups, AChE and thyroglobulin levels increased and decreased respectively from birth to attain normal adult levels from 6 months. Levels of iron and ferritin were higher in the first 6 month period for all infant groups studied, intersecting with vitamin C levels peaking around 4 months of age.
Conclusion:  Lower AChE levels and higher combined levels of iron and vitamin C in the first 6 months of life may augment cholinergic and oxidative stress effect, particularly at the age when SIDS is most prevalent. This may contribute to risk of ALTE and SIDS/SUDI events during infancy.     

Development of natural killer cytotoxicity during childhood: marked increases in number of natural killer cells with adequate cytotoxic abilities during infancy to early childhood.

The cytotoxicity of natural killer (NK) cells against K562 cells and their responsiveness to interferon-alpha and interleukin 2 (IL-2) were studied throughout childhood using 51Cr-release and single-cell assays. Although NK activity was extremely low in the neonatal period, it almost reached the adult level during 1 to 5 mo of age and remained at that level thereafter. At the single-cell level, the binding, lytic, and recycling abilities were also depressed in the neonatal period, but these abilities improved conspicuously after this period; in particular, the lysis and recycling were at higher levels during 6 mo to 4 y of age. The absolute numbers of circulating cytotoxic NK cells were high during infancy to early childhood: they were 54 +/- 24 (mean +/- SD/mm3) in neonates, 115 +/- 48 in 1- to 5-mo-old infants, 121 +/- 42 in 6- to 12-mo-old infants, 93 +/- 26 in 1- to 4-y-old children, and 42 +/- 16 in adults. Interferon-alpha and IL-2 could enhance NK activity throughout childhood. The IL-2 enhancement was prominent especially in the neonatal period; IL-2 yielded a 2.5-fold increase in the number of cytotoxic cells and improved the recycling to the adult level. At older ages, interferon-alpha and IL-2 yielded 1.4- and 1.9-fold increases in the number of cytotoxic cells, respectively, but did not enhance the recycling. The increased number of NK cells with adequate cytotoxic abilities during infancy to early childhood indicates the predominance of NK immunity during these periods. IL-2 is a cytokine that induces high levels of NK cytotoxicity even in neonates.     

Assessment of antioxidant reserves and oxidative stress in cerebrospinal fluid after severe traumatic brain injury in infants and children

Studies in experimental traumatic brain injury (TBI) support a key role for oxidative stress. The degree of oxidative injury in clinical TBI, however, remains to be defined. We assessed antioxidant defenses and oxidative stress in pediatric TBI by applying a comprehensive battery of assays to cerebrospinal fluid samples. Using a protocol approved by our institutional review board, 87 cerebrospinal fluid samples from 11 infants and children with severe TBI (Glasgow Coma Scale score < or = 8) and 8 controls were studied. Cerebrospinal fluid was drained as standard care after TBI. CSF was assessed on d 1, 2, and 5-7 after ventricular drain placement. Biochemical markers of oxidative stress included F(2)-isoprostane and protein sulfhydryl (detected by ELISA and fluorescence assay, respectively). Antioxidant defenses were measured by determination of total antioxidant reserve (via chemiluminescence assay), and ascorbate (via HPLC) and glutathione (via fluorescence assay) concentrations. Free radical production (ascorbate radical) was assessed by electron paramagnetic resonance spectroscopy. F(2)-isoprostane was markedly increased versus control, maximal on d 1 (93.8 +/- 30.8 pg/mL versus 7.6 +/- 5.1 pg/mL, p < 0.05). Total antioxidant reserve was reduced versus control. Reduction was maximal on d 5-7 (81.8 +/- 3.7 microM versus 178.9 +/- 2.2 microM, p < 0.05). Ascorbate was remarkably reduced (53.8 +/- 8 microM versus 163.8 +/- 21 microM on d 1, p < 0.05). Ascorbate depletion was likely associated with its free radical oxidation, as evidenced by electron paramagnetic resonance spectroscopy. Glutathione levels increased on d 1, then decreased versus control (0.19 +/- 0.05 microM versus 1.2 +/- 0.16 microM, p < 0.05). This is the first comprehensive study of antioxidant reserve and oxidative injury in clinical TBI. Progressive compromise of antioxidant defenses and evidence of free radical-mediated lipid peroxidation are noted. These markers could be used to monitor antioxidant strategies in clinical trials.     

The ontogeny of serum immunoreactive pancreatic lipase and cationic trypsinogen in the premature human infant

We evaluated the development of the exocrine pancreas in 16 healthy preterm infants (29.3 +/- 1.6 weeks). The infants were fed breast milk with formula supplements (n = 8) or formula alone (n = 8). Growth was monitored weekly for 12 weeks then at 3, 6, 9, 12 months. At the same intervals sera were determined for pancreatic lipase and cationic trypsinogen. In addition, cord blood samples were analysed from another 33 preterm (27.6 +/- 5.2 weeks) and 75 healthy full-term infants. Serum pancreatic lipase in the cord blood of term (3.7 +/- 0.4 micrograms/l) and preterm infants (1.8 +/- 0.2 micrograms/l) was significantly below values reported for older children (10.5 +/- 0.9 micrograms/l; p less than 0.001). In the preterm infant, serum lipase was also significantly lower than values obtained at term (p less than 0.001). At birth, serum trypsinogen for preterm (16.8 +/- 1.3 micrograms/l) and term infants (23.3 +/- 1.9 micrograms/l) were below those for older children (31.4 +/- 3.7 micrograms/l; p less than 0.05). Over the first 3 weeks of life, serum lipase and trypsinogen increased significantly. From 3 weeks to 12 months of age, serum trypsinogen values remained unchanged, but serum lipase increased dramatically after 10 weeks of age. Thus, at 6 and 12 months of age, the preterm infants had significantly higher serum lipase values than infants of the same age born at term. These two pancreatic enzymes appear to show independent age-related maturation in infants born before term. The rate of maturation of lipase appears to be accelerated by exposure to the extrauterine environment.     

Body composition in infants with chronic lung disease after treatment with dexamethasone

The aim of this study was to study the effect of chronic lung disease (CLD) and dexamethasone treatment on body composition in preterm infants (birthweight < 1500 g). In addition, anthropometric measurement of body composition were compared with dual-energy X-ray absorptiometry (DXA). Fourteen preterm infants with CLD and a comparison group of 18 preterm infants were studied until 3 mo corrected age. CLD infants received approximately 20 kcal kg-1 per day extra nutritional intake during dexamethasone treatment until term. At term no differences were found between CLD and no CLD infants for percentage bone mass (1.4 +/- 0.2 vs 1.4 +/- 0.1%), fat mass (18.7 +/- 4.5 vs 17.4 +/- 3.5%), lean body mass (79.9 +/- 4.6 vs 81.2 +/- 3.5%) or bone mineral density (0.15 +/- 0.02 vs 0.15 +/- 0.01%). At 3 mo corrected age both groups were also similar for bone mass (1.6 +/- 0.1 vs 1.6 +/- 0.2%), fat mass (22.6 +/- 5.5 vs 24.5 +/- 5.7%), lean body mass (75.8 +/- 5.7 vs 74.0 +/- 5.8%) and bone mineral density (0.20 +/- 0.02 vs 0.20 +/- 0.01%). All anthropometric measurements showed a high correlation with body composition. However, calculated fat mass was 56.7 +/- 8.8% lower than fat mass measured with DXA. CONCLUSION: Body composition at term and 3 mo corrected age in preterm infants treated with dexamethasone for CLD, who received extra caloric intake until term, did not differ from that in preterm infants without CLD.     

Vitamin K status of lactating mothers, human milk, and breast-feeding infants

Hemorrhagic disease of the newborn is a disease of breast-feeding newborns. There is little information on longitudinal breast milk concentrations of phylloquinone (vitamin K1) or the effects of maternal phylloquinone supplements on breast milk. In study part 1, 11 lactating mothers, who received 20 mg of phylloquinone orally, had rises in plasma (less than 1 to 64.2 +/- 31.5 ng/mL by 6 hours) and breast milk concentrations (from 1.11 +/- 0.82 to 130 +/- 188 ng/mL by 12 hours). In part 2, 23 lactating mothers and their infants were observed longitudinally along with a formula-fed control group of infants (n = 11). Mean breast milk concentrations of phylloquinone at 1, 6, 12, and 26 weeks were 0.64 +/- 0.43, 0.86 +/- 0.52, 1.14 +/- 0.72, and 0.87 +/- 0.50 ng/mL, respectively, in the infants fed human milk. Maternal phylloquinone intakes (72-hour dietary recalls) exceeded the recommended daily allowance of 1 microgram/kg per day. Infant phylloquinone intakes did not achieve the recommended daily allowance of 1 microgram/kg per day in any infant. Plasma phylloquinone concentrations in the infants fed human milk remained extremely low (mean less than 0.25 ng/mL) throughout the first 6 months of life compared with the formula-fed infants (4.39 to 5.99 ng/mL). In this small sample, no infant demonstrated overt vitamin K deficiency. Despite very low plasma phylloquinone concentrations, vitamin K supplements (other than in the immediate newborn period) cannot be recommended for exclusively breast-fed infants based on these data.     

Effect of human breast milk on urinary 8-hydroxy-2'-deoxyguanosine excretion in infants

During the perinatal period, oxidative stress is intimately involved in pathologic processes of serious diseases. Although breast milk contains many antioxidants, it is not clear whether breast milk can act as an antioxidant in infants in vivo. We compared the oxidative stress levels in total of 41 healthy 1-mo-old infants by measuring urinary 8-hydroxy-2'-deoxyguanosine, which is one of the biomarkers of oxidative DNA damage. These infants were divided into four groups according to the type of feeding. Urinary 8-hydroxy-2'-deoxyguanosine excretion of the breast-fed group was significantly lower than those of the artificial milk dominant mixed-fed group or the bottle-fed group. Our data suggest that breast milk, not artificial formula, acts as an antioxidant during infancy.     

Copper status of very low birth weight infants during the first 12 months of infancy.

The Cu intake and status of 106 very low birth weight (VLBW) infants (birth weight 1152 +/- 251 g, gestational age 29 +/- 3 wk, mean +/- SD) were determined approximately 1 mo before hospital discharge, at discharge (time 0), and at 3, 6, 9, and 12 mo +/- 3 wk corrected for gestational age. Infants were fed either formula plus supplemental Zn/Cu (SUPPL, n = 29); formula plus placebo (PLAC, n = 26); or a low birth weight formula (LBWF, n = 26) or were breast-fed (BRMLK, n = 25). Plasma Cu levels in the formula-fed infants increased significantly at each time period with no significant differences between feeding groups. Hair Cu was significantly higher in the SUPPL group compared to the PLAC, LBWF, and BRMLK groups at 3 and 6 mo. Erythrocyte Cu,Zn-superoxide dismutase (CuZnSOD) activity was lowest in the PLAC group. Cu intake was positively correlated with both hair Cu (r = 0.291, p less than 0.0001) and erythrocyte CuZnSOD activity (r = 0.281, p less than 0.001) but not with plasma Cu. An increasing number of formula-fed infants had very low CuZnSOD activity (less than 2 SD below mean) with increasing age (n = 1, 2, 8, 11, and 13 infants at times 0, 3, 6, 9, and 12 mo, respectively). At 12 mo, approximately one third of the formula-fed VLBW infants in this study had low Cu status as assessed by CuZnSOD activity. Infants with the lowest CuZnSOD activity were those with the largest weight gains from 0 to 6 mo and were observed in all formula-fed groups.(ABSTRACT TRUNCATED AT 250 WORDS)