Growth and development of premature infants fed predominantly human milk, predominantly premature infant formula, or a combination of human milk and premature formula
Authors
O'Connor, Deborah L.Jacobs, Joan
Hall, Robert
Adamkin, David
Auestad, Nancy
Castillo, Marcella
Connor, William E.
Connor, Sonja L.
Fitzgerald, Katherine A.
Groh-Wargo, Sharon
Hartmann, E. Eugenie
Janowsky, Jeri
Lucas, Alan
Margeson, Dean
Mena, Patricia
Neuringer, Martha
Ross, Gail
Singer, Lynn
Stephenson, Terence
Szabo, Joanne
Zemon, Vance
UMass Chan Affiliations
Department of Molecular Genetics and MicrobiologyDepartment of Medicine, Division of Infectious Diseases and Immunology
Document Type
Journal ArticlePublication Date
2003-09-26Keywords
AdultCognition
Ethnic Groups
Female
Hospitalization
Humans
*Infant Formula
*Infant Nutritional Physiological Phenomena
Infant, Newborn
Infant, Premature
Language Development
Male
Maternal Age
*Milk, Human
Motor Skills
Time Factors
Visual Acuity
Immunology and Infectious Disease
Metadata
Show full item recordAbstract
BACKGROUND: In a recent meta-analysis, human milk feeding of low birth-weight (LBW) infants was associated with a 5.2 point improvement in IQ tests. However, in the studies in this meta-analysis, feeding regimens were used (unfortified human milk, term formula) that no longer represent recommended practice. OBJECTIVE: To compare the growth, in-hospital feeding tolerance, morbidity, and development (cognitive, motor, visual, and language) of LBW infants fed different amounts of human milk until term chronologic age (CA) with those of LBW infants fed nutrient-enriched formulas from first enteral feeding. METHODS: The data in this study were collected in a previous randomized controlled trial assessing the benefit of supplementing nutrient-enriched formulas for LBW infants with arachidonic acid and docosahexaenoic acid. Infants (n = 463, birth weight, 750-1,800 g) were enrolled from nurseries located in Chile, the United Kingdom, and the United States. If human milk was fed before hospital discharge, it was fortified (3,050-3,300 kJ/L, 22-24 kcal/oz). As infants were weaned from human milk, they were fed nutrient-enriched formula with or without arachidonic and docosahexaenoic acids (3,300 kJ/L before term, 3,050 kJ/L thereafter) until 12 months CA. Formula fed infants were given nutrient-enriched formula with or without added arachidonic and docosahexaenoic acids (3,300 kJ/L to term, 3,050 kJ/L thereafter) until 12 months CA. For the purposes of this evaluation, infants were categorized into four mutually exclusive feeding groups: 1) predominantly human milk fed until term CA (PHM-T, n = 43); 2) >/= 50% energy from human milk before hospital discharge (>/= 50% HM, n = 98); 3) < 50% of energy from human milk before hospital discharge (< 50% HM, n = 203); or 4) predominantly formula fed until term CA (PFF-T, n = 119). RESULTS: PFF-T infants weighed approximately 500 g more at term CA than did PHM-T infants. This absolute difference persisted until 6 months CA. PFF-T infants were also longer (1.0-1.5 cm) and had larger head circumferences (0.3-1.1 cm) than both PHM-T and >/= 50% HM infants at term CA. There was a positive association between duration of human milk feeding and the Bayley Mental Index at 12 months CA (P = 0.032 full and P = 0.073 reduced, statistical models) after controlling for the confounding variables of home environment and maternal intelligence. Infants with chronic lung disease fed >/= 50% HM until term CA (n = 22) had a mean Bayley Motor Index about 11 points higher at 12 months CA compared with infants PFF-T (n = 24, P = 0.033 full model). CONCLUSION: Our data suggest that, despite a slower early growth rate, human milk fed LBW infants have development at least comparable to that of infants fed nutrient-enriched formula. Exploratory analysis suggests that some subgroups of human milk fed LBW infants may have enhanced development, although this needs to be confirmed in future studies.Source
J Pediatr Gastroenterol Nutr. 2003 Oct;37(4):437-46.Permanent Link to this Item
http://hdl.handle.net/20.500.14038/35266PubMed ID
14508214Related Resources
Link to Article in PubMedCollections
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Role of multiple births in very low birth weight and infant mortalityMagee, B. Dale (2004-10-01)OBJECTIVE: To determine the percentage of very-low-birth-weight (VLBW) infants (g) and infant deaths attributable to multiple births in the general population and in women aged 35+. STUDY DESIGN: The year 2000 Massachusetts birth certificate database with linked births-deaths was examined. Etiologic fractions (EF) for VLBW and infant mortality attributable to multiples were calculated for the general population and the 35+ age group. The percentages of multiples occurring in the 35+ age group were calculated. Infant deaths due to congenital anomalies and "perinatal conditions" were calculated. RESULTS: There were 81,582 resident births in Massachusetts in 2000. Of them 4.3% were multiples. Of the 1090 VLBW infants, 26.1% (95% CI: 23.5-28.8) were in twins and 7.7% (95% CI: 6.2-9.5) in higher-order multiples, yielding an EF of 30.8% for multiples in VLBW. In the 35+ age group, the multiple birth ratio was 6.6% (95% CI: 6.3-7.0). The EF for multiples and VLBW in this age group was 33.7%. The 35+ age group accounted for 32.4% (95% CI: 30.8-34.0) of twins and 45.5% (95% CI: 39.1-52.0) of higher-order multiples born in 2000. Of the 392 infant deaths, 57 (14.6%; 95% CI: 11.2-18.4) were attributed to congenital anomalies, and 236 (60.2%; 95% CI: 55.2-65.0) to "perinatal conditions." Multiples were responsible for 8 (14%; 95% CI: 6.3-25.8) of deaths due to anomalies, and 73 (30.9%; 95% CI: 25.1-37.3) due to "perinatal conditions." CONCLUSION: Over 30% of VLBW infants, nearly 20% of infant mortality and >30% of infant mortality due to perinatal conditions could be attributed to multiples. Multiple pregnancy is a significant public health problem.
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Role of smoking in low birth weightMagee, B. Dale; Hattis, Dale; Kivel, Nancy M. (2004-01-01)OBJECTIVE: To assess the role of smoking on low birth weight (LBW). STUDY DESIGN: From Massachusetts for 1998, 79,904 birth certificates were reviewed. Birth weight, gestational age, plurality and maternal race were analyzed in relation to the mother's smoking status during the pregnancy. The etiologic fraction (EF) was calculated for smoking and LBW for the group as a whole as well as for various subgroups. RESULTS: A total of 11.7% of women acknowledged smoking during pregnancy. The overall LBW rate was 6.83%. The relative risk (RR) of LBW among smokers was 1.58. For all births the EF for smoking was 6.4% (95% CI: 5.4-7.3). For singleton pregnancies it was 10.9% (95% CI: 9.6-12.1) (14% for singleton whites and 7.2 for singleton blacks). At term, the EF of smoking on LBW was 13.4% (95% CI: 11.5-15.3), with an EF of 16.7% (95% CI: 14.5-18.7) for term singletons (21.4% among whites and 14.6% among blacks). Among very LBW infants, smoking accounted for 1.7% (95% CI:--0.5-3.8) of the outcome (5.8% among singletons). When stratifying for the effect of smoking, the rate of LBW was 6.38% among nonsmokers, 9.5% (RR 1.48, 1.38-1.61) among light smokers, 11.67% (RR 1.82, 1.63-2.05) among moderate smokers and 11.72% (RR 1.84, 1.33-2.54) among heavy smokers. Sixty percent of the overall population effect of smoking on LBW was in the category of light smokers. CONCLUSION: The amount of LBW attributable to smoking was 6.4% in this sample. Among those who smoked, LBW was 58% more likely than among nonsmokers, and 60% of the overall population effect of smoking on LBW was noted among light smokers.
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Chronic lung disease and developmental delay at 2 years of age in children born before 28 weeks' gestationLaughon, Matthew; O'Shea, Michael T.; Allred, Elizabeth N.; Bose, Carl; Kuban, Karl C.K.; Van Marter, Linda J.; Ehrenkranz, Richard A.; Leviton, Alan; ELGAN Study Investigators; Bednarek, Francis; et al. (2009-08-22)INTRODUCTION: Extremely low gestational age newborns (ELGANs) are at increased risk of chronic lung disease (CLD) and of developmental delay. Some studies have suggested that CLD contributes to developmental delay. PATIENTS AND METHODS: We examined data collected prospectively on 915 infants born before the 28th week of gestation in 2002-2004 who were assessed at 24 months of age with the Bayley Scales of Infant Development-2nd Edition or the Vineland Adaptive Behavior Scales. We excluded infants who were not able to walk independently (Gross Motor Function Classification System score < 1) and, therefore, more likely to have functionally important fine motor impairments. We defined CLD as receipt of oxygen at 36 weeks' postmenstrual age and classified infants as either not receiving mechanical ventilation (MV) (CLD without MV) or receiving MV (CLD with MV). RESULTS: Forty-nine percent of ELGANs had CLD; of these, 14% were receiving MV at 36 weeks' postmenstrual age. ELGANs without CLD had the lowest risk of a Mental Developmental Index (MDI) or a Psychomotor Developmental Index (PDI) of <55, followed by ELGANs with CLD not receiving MV, and ELGANs with CLD receiving MV (9%, 12%, and 18% for the MDI and 7%, 10%, and 20% for the PDI, respectively). In time-oriented multivariate models, the risk of an MDI of <55 was associated with the following variables: gestational age of <25 weeks; single mother; late bacteremia; pneumothorax; and necrotizing enterocolitis. The risk of a PDI of <55 was associated with variables such as single mother, a complete course of antenatal corticosteroids, early and persistent pulmonary dysfunction, pulmonary deterioration during the second postnatal week, pneumothorax, and pulmonary interstitial emphysema. CLD, without or with MV, was not associated with the risk of either a low MDI or a low PDI. However, CLD with MV approached, but did not achieve, nominal statistical significance (odds ratio: 1.9 [95% confidence interval: 0.97-3.9]) for the association with a PDI of <55. CONCLUSIONS: Among children without severe gross motor delays, risk factors for CLD account for the association between CLD and developmental delay. Once those factors are considered in time-oriented risk models, CLD does not seem to increase the risk of either a low MDI or a low PDI. However, severe CLD might increase the risk of a low PDI.