ABSTRACT
BACKGROUND: Evidence-based practice guidelines for aggressive nutritional intervention by using parenteral amino acids (AAs) and minimal enteral feeding (MEF) as early as the first day of life have not been tested for benefits to bone mass. OBJECTIVE: We investigated whether early introduction of parenteral AAs and MEF improves growth and bone mass achieved by term age in infants born prematurely. DESIGN: Twenty-seven infants who were < or = 1200 g and < or = 32 wk gestation at birth were randomly assigned by using a 2 x 2 design to treatment of either 1 g AAs/kg within the first 24 h or 12 mL MEF x kg(-1) x d(-1) within the first 72 h of life. Nutrition and growth were documented during hospitalization, and bone mineral content (BMC) of lumbar spine 1-4, femur, and whole body was measured at term age. Biomarkers of bone metabolism were measured at weeks 1, 3, and 5 and at discharge. Statistical analysis was conducted by using 2 x 2 analysis of variance for intent to treat and for infants receiving protocol nutrition. RESULTS: Over the first 14 d of life, a main effect of early AAs elevated total intake of protein, and a main effect of early MEF was a higher frequency of MEF volumes exceeding > 12 mL x kg(-1) x d(-1). Main effects on growth were not evident. An interaction effect was observed for osteocalcin whereby early AAs or MEF alone elevated osteocalcin. A main effect of early MEF yielded higher BMC of spine and femur. CONCLUSION: Early aggressive nutrition support with MEF enhances BMC in premature infants, but early MEF or AAs do not improve growth.
Subject(s)
Amino Acids/administration & dosage , Bone Density/drug effects , Enteral Nutrition , Infant, Premature/physiology , Infant, Very Low Birth Weight/physiology , Parenteral Nutrition , Absorptiometry, Photon , Amino Acids/therapeutic use , Analysis of Variance , Bone Development/drug effects , Bone Development/physiology , Female , Gestational Age , Growth/drug effects , Humans , Infant Nutritional Physiological Phenomena , Infant, Newborn , Infant, Premature/growth & development , Infant, Very Low Birth Weight/growth & development , Male , Osteocalcin/bloodABSTRACT
Long-chain polyunsaturated fatty acids (LC PUFA) are associated with bone mass in animals and human adults, yet no data exist for human infants. Thus, the objective of this study was to establish that LC PUFA status is associated with bone mass in healthy infants. Thirty mother-infant pairs were studied for LC PUFA status by measuring maternal and cord blood red blood cells (RBC) for arachidonic acid (AA), eicosapentaenoic acid (EPA), and DHA. Infant anthropometry and lumbar spine 1-4, femur and whole-body bone mineral content (BMC) were measured within 15 d of delivery. Maternal and infant LC PUFA were tested for their relationship to BMC using Pearson correlation and backward step-wise regression analyses. At birth, the average gestational age was 39.3+/-1.1 wk and body weight was 3433+/-430 g. Cord RBC AA was positively correlated with whole-body BMC, AA:EPA positively correlated with lumbar spine 1-4 BMC and femur BMC. Maternal RBC AA was positively correlated with whole-body BMC. After accounting for infant weight using regression, whole-body BMC was positively predicted by cord RBC AA but none of the maternal LC PUFA; lumbar spine 1-4 BMC was positively predicted by cord RBCAA:EPA ratio but negatively by maternal DHA; and femur BMC was not predicted by cord LC PUFA but was negatively predicted by maternal DHA. Imbalances among the n-6 and n-3 LC PUFA by term gestation are associated with lower bone mass, suggesting that the maternal diet should be balanced in n-6 and n-3 LC PUFA.
Subject(s)
Bone Density , Fatty Acids, Unsaturated/blood , Fetal Blood/chemistry , Infant, Newborn/growth & development , Anthropometry , Bone and Bones/anatomy & histology , Erythrocytes/chemistry , Female , Fetal Blood/cytology , Gestational Age , Humans , Infant, Newborn/blood , Male , PregnancyABSTRACT
BACKGROUND: Vitamin D is required for normal bone growth and mineralization. We sought to determine whether vitamin D deficiency at birth is associated with bone mineral content (BMC) of Canadian infants. METHODS: We measured plasma 25-hydroxyvitamin D [25(OH)D] as an indicator of vitamin D status in 50 healthy mothers and their newborn term infants. In the infants, anthropometry and lumbar, femur and whole-body BMC were measured within 15 days of delivery. Mothers completed a 24-hour recall and 3-day food and supplement record. We categorized the vitamin D status of mothers and infants as deficient or adequate and then compared infant bone mass in these groups using nonpaired t tests. Maternal and infant variables known to be related to bone mass were tested for their relation to BMC using backward stepwise regression analysis. RESULTS: Twenty-three (46%) of the mothers and 18 (36%) of the infants had a plasma 25(OH)D concentration consistent with deficiency. Infants who were vitamin D deficient were larger at birth and follow-up. Absolute lumbar spine, femur and whole-body BMC were not different between infants with adequate vitamin D and those who were deficient, despite larger body size in the latter group. In the regression analysis, higher whole-body BMC was associated with greater gestational age and weight at birth as well as higher infant plasma 25(OH)D. CONCLUSION: A high rate of vitamin D deficiency was observed among women and their newborn infants. Among infants, vitamin D deficiency was associated with greater weight and length but lower bone mass relative to body weight. Whether a return to normal vitamin D status, achieved through supplements or fortified infant formula, can reset the trajectory for acquisition of BMC requires investigation.
Subject(s)
Bone Density , Vitamin D Deficiency/physiopathology , Vitamin D/analogs & derivatives , Adult , Body Height , Body Weight , Dietary Supplements , Female , Femur/physiology , Gestational Age , Humans , Infant, Newborn , Linear Models , Male , Vitamin D/bloodABSTRACT
We summarize here the evidence indicating that carbon from alpha-linolenate and linoleate is readily recycled into newly synthesized lipids. This pathway consumes the majority of these fatty acids that is not beta-oxidized as a fuel. Docosahexaenoate undergoes less beta-oxidation and carbon recycling than do alpha-linolenate or linoleate, but is it still actively metabolized by this pathway? Among polyunsaturates, arachidonate appears to undergo the least beta-oxidation and carbon recycling, an observation that may help account for the resistance of brain membranes to loss of arachidonate during dietary deficiency of n-6 polyunsaturates. Preliminary evidence suggests that de novo lipid synthesis consumes carbon from alpha-linolenate and linoleate in preference to palmitate, but this merits systematic study. Active beta-oxidation and carbon recycling of 18-carbon polyunsaturates does not diminish the importance of being able to convert alpha-linolenate and linoleate to long-chain polyunsaturates but suggests that a broad perspective is required in studying the metabolism of polyunsaturates in general and alpha-linolenate and linoleate in particular.