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Article

The Impact of Enteral Nutrition Type, Volume, and Time of Introduction on the Risk of Growth Failure and Bronchopulmonary Dysplasia in Preterm Infants

by
Karen D. Hendricks-Muñoz
1,2,*,
Miheret S. Yitayew
1,2,
Nayef Chahin
1,2,
Allison Williams
1,
Jie Xu
1,
Adeola Abdulkadir
3,
Bemnet Alemayehu
1 and
Judith A. Voynow
1,2
1
Virginia Commonwealth University School of Medicine, Richmond, VA 23298, USA
2
Children’s Hospital of Richmond at VCU, Richmond, VA 23298, USA
3
Eastern Virginia Medical School, Norfolk, VA 23501, USA
*
Author to whom correspondence should be addressed.
Nutrients 2026, 18(2), 283; https://doi.org/10.3390/nu18020283
Submission received: 4 December 2025 / Revised: 6 January 2026 / Accepted: 13 January 2026 / Published: 16 January 2026
(This article belongs to the Special Issue Perinatal Outcomes and Early-Life Nutrition)
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Abstract

Background/Objectives: Greater than 50% of surviving very preterm infants are affected by postnatal growth failure and are at high risk of associated development of bronchopulmonary dysplasia (BPD). Given the influence of enteral feeding on growth failure, we aimed to determine the impact of type, volume, and time of introduction of enteral feeds on mitigating the risk of postnatal growth failure and BPD risk. Methods: This was a retrospective chart review of mothers’ own milk (MOM), pooled pasteurized donor human milk (PDHM) feeding, postnatal growth, and BPD severity in preterm infants <33 weeks of gestation admitted to the Children’s Hospital of Richmond at VCU neonatal intensive care unit between 2021 and 2024. Statistical analysis included linear regression with moderation analysis using the Hayes Process model, chi-square tests, linear and multinomial logistic regression, with p-value < 0.05 considered significant. Results: After controlling for the percentage of MOM received at 34 weeks corrected gestational age (cGA), greater severity of BPD was associated with lower infant weight and growth failure, p < 0.001. Early introduction of MOM (3 days of life) and greater volume of MOM showed better linear growth and decreased risk of severe BPD, respectively (p < 0.001). Conclusions: Provision of MOM to preterm infants within 3 days of life was associated with a moderation of the relationship between gestational age and growth velocity, with improved growth velocity trajectory. Preterm infants who received a greater volume of MOM through 34 weeks cGA experienced less severe BPD compared to those fed higher volumes of PDHM. As the incidence of growth failure paralleled the incidence of BPD severity, identification of key MOM components becomes important to address and augment the value of PDHM in the management of preterm infants.

1. Introduction

Very preterm infants (vPT) <33 weeks gestation, account for 52% of infant deaths, with >50% affected by postnatal growth failure [1,2]. Growth failure during infancy is a major global problem with associated adverse effects on long-term infant health, including lung and neurodevelopment [3,4]. Mother’s own milk (MOM) is a nutrient source that not only influences preterm infant mortality but also attenuates morbidities from necrotizing enterocolitis, chronic lung disease, and adverse neurodevelopment [5,6,7,8]. Chronic Lung Disease during infancy or bronchopulmonary dysplasia (BPD), a major global problem with life-long morbidities, is a multifactorial disease of disrupted alveolarization and pulmonary vascular development, and impaired lung growth [9,10,11,12]. BPD remains the most common long-term complication of prematurity in those infants < 32 weeks of gestation, which affects not only the respiratory system but also overall growth and development in preterm survivors beyond the neonatal period, extending into childhood and adolescence [12,13,14]. Breastmilk appears to offer lung and immune protective benefits against BPD, allergies, and later childhood asthma [15,16,17,18,19,20,21].
In addition to its protective role against BPD, MOM has been shown to positively impact postnatal growth compared to pasteurized donor human milk (PDHM), often used as a substitute or bridge for feeding the PT infant [22,23,24]. Lund et al. observed that increased intake of MOM compared to PDHM was associated with improved postnatal weight gain and head circumference growth in extremely preterm infants [25].
While human milk is a cornerstone of neonatal nutrition and the nutritional components of human milk have been well described and known to enhance healthy immune development, when a mother’s own milk (MOM) is unavailable, pasteurized donor human milk (PDHM) is commonly used. While PDHM confers protection against necrotizing enterocolitis, it differs substantially from MOM in bioactive composition, and its impact on lung development and growth remains incompletely understood [26,27,28,29,30,31]. Additionally, the influence of early milk colostrum and transitional MOM composition is unique compared to mature PDHM, with limited understanding of this influence on growth or BPD development [32,33,34,35]. Thus, we hypothesized that early (within the first week of life) and sustained exposure to MOM favorably modifies the effects of gestational immaturity and early illness severity (SNAPPE-II) on infant postnatal growth velocity trajectories and reduces the severity of bronchopulmonary dysplasia that would align with growth impairment [36].
Given the influence of breast milk on growth failure and BPD, this study aimed to address a critical knowledge gap by defining how timing and cumulative dose of MOM as compared to PDHM modify the effects of gestational immaturity and illness severity on postnatal growth and BPD, as well as identify any association of BPD risk with growth.

2. Materials and Methods

2.1. Study Design and Participants

This study was conducted at the Children’s Hospital of Richmond at Virginia Commonwealth University and involved a retrospective analysis of a cohort from a prospective longitudinal observational study. The cohort included infants born at less than 33 weeks of gestation who were enrolled in an Institutional Review Board-approved study (HM20022431). Preterm infants under 33 weeks of gestation and their mothers, regardless of their gender, race, or ethnicity, were included. Exclusions were made for infants with known chromosomal anomalies or major birth defects, or those without written consent.
Infants received feeding according to protocol, initiated upon the receipt of the mother’s milk or, at the mother’s discretion, from PDHM. The volume was advanced based on gestational age, birth weight, and feeding tolerance. Mother’s own milk was collected and stored in containers for immediate use or frozen until provided to the infant, with administration conducted in the order the milk was received. Pasteurized donor human milk was sourced from the King’s Daughters Milk Bank in Norfolk, VA, USA, which operates under the accreditation of the Human Milk Banking Association of North America (HMBANA). All PDHM was barcoded, cultured negatively, and had documented fat, protein, carbohydrates, total solids, and energy.

2.2. Clinical Data and Outcomes

Clinical and demographic data were acquired using electronic medical records, capturing information on gender, maternal race and health conditions, gestational age (GA), birthweight (BW), and the type of enteral feeding (MOM or PDHM), as well as feeding volume and timing of introduction. Growth failure was defined as an infant’s weight below the 10th and 3rd percentiles at 34 weeks corrected GA, based on the Fenton infant growth scale [37]. BPD was documented and defined according to the classification established by Jensen et al. This classification assesses disease severity based on the mode of respiratory support received at 36 weeks postmenstrual age, regardless of the use of supplemental oxygen. At 36 weeks corrected GA, BPD severity is categorized as follows: Grade 1 requires ≤2 L/min nasal cannula (classified as mild), Grade 2 involves >2 L/min nasal cannula or non-invasive ventilation (classified as moderate), and Grade 3 includes infants requiring invasive mechanical ventilation (classified as severe) [11]. The severity of health illness was evaluated using the SNAPPE-II [36].

2.3. Statistical Analysis

Subject characteristics were summarized using frequencies and percentages or means and standard deviations. The statistical analysis employed linear regression with moderation analysis, utilizing the Hayes PROCESS model, adjusted for infant health severity, as well as Pearson correlations. Sample size and power calculations were performed to detect a relationship at 80% power, establishing a minimum sample size of 29 per group, resulting in a total of 58 mother–infant pairs needed to assess the relationship between growth restriction, diet, and BPD risk. All analyses were conducted with significance defined at a p-value of <0.05, using SAS Version 9.4 Statistical Software (SAS Institute, Cary, NC, USA).
Directed acyclic graphs (DAGs) were constructed to guide covariate selection using the DAGitty tool v3.1 (https://dagitty.net/dags.html, 23 December 2025) [38,39]. Based on these diagrams, gestational age and SNAPPE-II score were identified as the minimal sufficient adjustment set, capturing baseline immaturity and illness severity that influence both feeding exposure and clinical outcomes. Variables occurring downstream of milk exposure, such as respiratory support or feeding advancement, were not adjusted to avoid overadjustment bias.

3. Results

3.1. Covariate Selection with Directed Acyclic Graph Assessment

Using directed acyclic graphs (DAGs) to guide covariate selection and analytic strategy, gestational age and SNAPPE-II score were identified as the minimal sufficient adjustment set, capturing baseline immaturity and illness severity that influence both milk exposure and clinical outcomes [38,39]. By avoiding adjustment for downstream mediators such as respiratory support or feeding advancement, we minimized overadjustment bias and preserved the interpretability of observed associations (Figure 1).

3.2. Infant Population Characteristics

There were 100 premature infants included in this analysis with a mean gestational age of 27.1 ± 1.5 weeks and a mean birth weight of 1151 ± 441 gms. Racial and ethnic composition included 37% White, 46% Black, and 6% Asian or Other categories, with 11% of the population of Hispanic ethnicity, see Table 1.

3.3. Infant Growth Failure and BPD Association

The characteristics of the infants with BPD are shown in Table 2. There was a total of 39 (39%) of infants with BPD, of which 21 (21%) were mild BPD and 18 (18%) were considered moderate/severe BPD. The mean gestational age of the infants with BPD was significantly younger and smaller than that of those who did not develop BPD. There were no significant racial or ethnic differences among the infants with BPD or with later growth failure. There were 41 infants (41%) with growth failure at 34 weeks cGA by weight of <10th percentile and 18 (18%) at <3rd percentile, of which there were greater association of BPD with infants with growth failure at the <10th percentile as well as at the <3rd percentile, Table 2.

3.4. Influence of MOM and PDHM on Growth Velocity

Moderations were conducted to examine whether early nutrition type (MOM vs. PHDM) moderated the risk of gestational age on growth velocity.
The first moderation examined MOM in the first three days as a moderator of the relationship between gestational age and growth velocity. The overall regression model was statistically significant, F (3, 179) = 8.41, p < 0.001, indicating that gestational age and the mother’s own milk explained 12.35% of the variance in growth velocity (R2 = 0.123). Gestational age was a significant negative predictor of growth velocity (b = −0.86, SE = 0.24, t = −3.66, p < 0.001, 95% CI [−1.32, −0.40]), indicating that lower gestational age was associated with lower growth velocity. Mothers’ own milk was not a significant predictor of growth velocity (b = −3.08, SE = 8.88, t = −0.35, p = 0.729). Importantly, the interaction between gestational age and mother’s own milk was significant (b = 0.41, SE = 0.23, t = 0.46, p = 0.046), which indicates that while mother’s own milk alone does not predict growth velocity, mother’s own milk does significantly attenuate the risk conferred by lower gestational age. The change in explained variance due to the interaction term was negligible (ΔR2 = 0.123), and the interaction significantly improved model fit.
The second moderation, which examined whether initiation of PDHM in the first 3 days moderated the risk between gestational age and growth velocity, was not significant. Subsequent moderations examining the moderating influence of MOM and PHDM after day of life 4 on the relationship between gestational age and growth were both not significant, as shown in Figure 2.

3.5. Influence of Volume of MOM and PDHM on Risk of BPD

Using Pearson correlations, we investigated the association of volume of MOM and PDHM on the influence of BPD severity risk. We noted that there was greater severity of BPD associated with lower volume of MOM, r = 0.156, p < 001, as shown in Figure 3. This association was not identified for PDHM, r = −0.031, p = 0.663.

3.6. Association of Growth Failure and Risk of BPD

We aimed to assess the association of growth failure and risk of BPD. After controlling for the % volume of MOM and PDHM at 34 weeks, we identified that greater severity of BPD was associated with lower infant weight and growth failure at 34 weeks cGA. Infant weight at 34 weeks was significantly correlated with BPD severity, such that more severe BPD was associated with lower infant weight at 34 weeks, p < 0.001, r(125) = −0.332, Figure 4.

4. Discussion

Human milk feeding in preterm infants improves feeding tolerance, supports gut health, and is associated with a reduction in the severity of bronchopulmonary dysplasia (BPD) [17,19,22,40,41]. Although human milk is considered the optimal source of nutrition, it does not fully meet the nutritional needs of the very preterm infant, necessitating the addition of micronutrient supplementation. When mother’s own milk (MOM) is not available, pooled pasteurized donor human milk (PDHM) from an accredited human milk bank is recommended [42,43]. However, studies have demonstrated greater postnatal growth restriction in infants fed PDHM compared to MOM [22,23,24]. Additionally, MOM remains the optimal nutritional source associated with a reduction in mortality and morbidities related to necrotizing enterocolitis, chronic lung disease, and adverse neurodevelopment owing to its immune-supporting composition that optimizes gut microbiome, intestinal integrity, and immune development [7,8,9,10,39,44,45,46].
In this study, we observed that exposure to MOM and not PDHM within the first three days of postnatal life was associated with greater growth velocity and attenuation of postnatal growth failure. Furthermore, the cumulative volume of MOM received during hospitalization was significantly associated with reduced BPD severity, while BPD risk was correlated with the degree of postnatal growth failure. These findings continue to support the preferential use of MOM utilization over PDHM in this high-risk population. Our findings differ from those of Avila-Alvarez et al., who reported no significant difference in BPD incidence among premature infants based on whether initial feedings consisted of MOM or PDHM [39]. Importantly, our study incorporated both timing and volume of MOM compared to PDHM, accounting for loss of early colostrum and transitional milk exposure, replete with bioactive components, as compared to substitution with mature PDHM as the initial feeding.
Our study is novel in identifying a relationship between postnatal growth failure and BPD severity. By linking milk exposure to both growth trajectories and pulmonary outcomes, this work bridges traditionally siloed domains of neonatal nutrition and respiratory medicine. Prior studies have demonstrated the nutritional benefits of human milk for very preterm infants and its potential protective role against BPD, allergic disease, and later childhood asthma [5,6,7,17,19,20,22,23,46,47]. Consistent with our findings, human milk feeding has repeatedly been associated with reduced BPD risk, though variability exists in reported effects of MOM versus PDHM on growth and BPD severity [26,46,48,49,50,51]. A 2019 meta-analysis demonstrated that exclusive feeding with unpasteurized MOM was associated with a significant reduction in BPD risk (RR 0.74, 95% CI 0.57–0.96) [7]. However, that analysis of 15 studies did not demonstrate a significant reduction in BPD oxygen requirement when infants were fed PDHM alone, with benefit observed primarily when MOM was supplemented with PDHM [7]. Similarly, a study comparing raw versus pasteurized MOM identified a significantly lower risk of BPD with raw MOM after adjustment for confounders (OR 0.40, 95% CI 0.27–0.67; p < 0.001) [52]. Another study reported that PDHM was associated with poorer weight gain and lower neurodevelopmental outcomes compared with MOM, without a significant difference in BPD risk; however, that study was not powered to assess BPD severity [53]. Collectively, these findings suggest that pasteurization and the loss of key bioactive, lipid, anti-inflammatory, and immune-modulating components in PDHM may contribute to observed differences in outcomes [8,53].
Our study had limitations that should be taken into account when interpreting these results. This was a single-center retrospective design study of a prospective cohort with PDHM sourced from one center that may limit the generalization of the results to other units with different populations or clinical practices of enteral feeding or management of BPD. This limitation is somewhat offset by the standard management of the cohort within the same neonatal unit and with guidelines in feeding and clinical care, and respiratory management of infants at risk of BPD. Additionally, while causality cannot be established in an observational study, we strengthened causal interpretability through causal modeling using gestational age and SNAPPE-II covariates, longitudinal data on the volume or proportion of MOM or PDHM received by the infants, as well as the time and initiation of each feeding type during hospital admission. This design is important as infants can receive some PDHM during their course in the NICU, and it was useful to unmask the differences between the PDHM and MOM groups to identify the impact of type, timing, and volume of feeding on health outcomes. These approaches reduce bias and support bio-logic plausibility without overstating causation. Rather than treating human milk as a uniform exposure, we explicitly test whether early MOM vs. PDHM exposure modifies the relationship between gestational age, growth, and BPD severity.
Our results underscore the importance of early-life exposure to MOM in potentially shaping growth trajectories and BPD development in the very preterm infant. Because not all infants have access to MOM for a variety of reasons, it is critical to identify the specific growth-promoting and BPD-modulating components of human milk and make them available to all infants when MOM is not feasible. Components absent or diminished in PDHM, such as microbiota, nutritional lipids, and bioactive factors, may influence both the establishment of the infant’s gut homeostasis and provide modulators of pulmonary immune and growth pathways. Given that nutrition is one of the few modifiable factors that clinicians can leverage to influence postnatal growth failure and risk of BPD, defining key compositional elements of MOM that mitigate BPD severity and growth failure is essential to advance precision-based personalized neonatal care of very preterm infants in the NICU.
Very preterm infants, 22–32 weeks of gestation, representing approximately 1.6% of all US live births, account for 52% of infant deaths, with more than 50% affected by extrauterine or postnatal growth failure [1,2,10,45]. For these infants, MOM or PDHM remains the preferred nutritional source to reduce mortality and morbidities, including necrotizing enterocolitis, chronic lung disease, and adverse neurodevelopment [5,6,7]. Our findings support the early implementation of MOM, as compared to PDHM, not only as an effective dietary strategy to promote optimal infant growth patterns but also as a means to reduce the risk of BPD and its associated long-term health consequences in very preterm infants.

5. Conclusions

Introduction of MOM within 3 days of life was associated with a moderation of the relationship between gestational age and growth velocity, and these results were associated with improved growth velocity trajectory in very preterm infants. Preterm infants who received a greater cumulative volume of MOM through 34 weeks corrected gestational age experienced less severe BPD compared to those fed PDHM. Given the identified association between postnatal growth failure and BPD severity, future research should focus on the identification of key MOM components responsible for these protective effects and on addressing the variability in outcomes associated with PDHM.

Author Contributions

Conceptualization: K.D.H.-M.; data curation: K.D.H.-M., A.W., J.X., A.A. and B.A.; formal analysis: K.D.H.-M., M.S.Y., N.C., A.W., J.X., A.A. and B.A.; funding acquisition: K.D.H.-M.; investigation: K.D.H.-M., J.X. and B.A.; methodology: K.D.H.-M., M.S.Y., J.X. and J.A.V.; project administration: K.D.H.-M., J.X. and J.A.V.; resources: K.D.H.-M.; supervision: K.D.H.-M. and J.X.; validation: K.D.H.-M. and J.X.; writing—original draft preparation: K.D.H.-M. and N.C.; writing—review and editing: K.D.H.-M., M.S.Y., N.C., A.W., J.X. and J.A.V. All authors have read and agreed to the published version of the manuscript.

Funding

This research was funded by The Gerber Foundation grant number 8451 to Karen D. Hendricks-Muñoz and Children’s Hospital of Richmond Division of Neonatal Medicine JACKS Summer Scholars FUND.

Institutional Review Board Statement

The study was conducted in accordance with the Declaration of Helsinki and approved by the Institutional Review Board of Virginia Commonwealth University School of Medicine (protocol code HM20022431_Ame1 7 January 2021).

Informed Consent Statement

Informed consent was obtained from all subjects involved in the study.

Data Availability Statement

No new data were created, and data are unavailable due to privacy or ethical restrictions.

Acknowledgments

The authors acknowledge the Children’s Hospital of Richmond Division of Neonatal Medicine JACKS Summer Scholars Program Funds in support of the extraction and analysis technical support of this study. The authors acknowledge that they have reviewed and edited the output and take full responsibility for the content of this publication.

Conflicts of Interest

The authors declare no conflicts of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Abbreviations

The following abbreviations are used in this manuscript:
MOMMother’s own milk
PDHMPasteurized Donor Human Milk
BPDBronchopulmonary dysplasia

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Nutrients 18 00283 g001
Figure 1. Directed acyclic graph (DAG) of analytic strategy. A directed acyclic graph characterizes the analytical strategy of the study where optimal growth influences BPD and optimal growth and BPD are independently influenced by early and cumulative MOM.
Figure 1. Directed acyclic graph (DAG) of analytic strategy. A directed acyclic graph characterizes the analytical strategy of the study where optimal growth influences BPD and optimal growth and BPD are independently influenced by early and cumulative MOM.
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Figure 2. The Impact of Timing of MOM on Growth Velocity. Adjusted for infant health severity using the SNAPPE-II score [36], the figure demonstrates the influence of MOM (a) after 3 days and (b) within 3 days of life on the moderation of the relationship between GA and growth velocity, including infants at growth failure risk.
Figure 2. The Impact of Timing of MOM on Growth Velocity. Adjusted for infant health severity using the SNAPPE-II score [36], the figure demonstrates the influence of MOM (a) after 3 days and (b) within 3 days of life on the moderation of the relationship between GA and growth velocity, including infants at growth failure risk.
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Figure 3. BPD Severity Impacted by Volume of MOM. After controlling for the percentage of MOM at 34 weeks cGA, a greater volume of MOM was associated with a lower severity of BPD.
Figure 3. BPD Severity Impacted by Volume of MOM. After controlling for the percentage of MOM at 34 weeks cGA, a greater volume of MOM was associated with a lower severity of BPD.
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Figure 4. The Influence of Growth Status on BPD Severity. After controlling for health severity using the SNAPPE-II score [36] and % MOM at 34 weeks, a greater severity of BPD was associated with a lower infant weight and growth failure at 34 weeks cGA.
Figure 4. The Influence of Growth Status on BPD Severity. After controlling for health severity using the SNAPPE-II score [36] and % MOM at 34 weeks, a greater severity of BPD was associated with a lower infant weight and growth failure at 34 weeks cGA.
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Table 1. Characteristics of the infant overall population.
Table 1. Characteristics of the infant overall population.
Characteristics
Gestational Age (weeks) ± SD27.1 ± 1.5
Birthweight (grams) ± SD1151 ± 441
Sex—Female n (%)55 (55)
Sex—Male n (%)45 (45)
Race and Ethnicity—n (%)
White37 (37)
Black46 (46)
Asian/Other6 (6)
Hispanic11(11)
Table 2. Characteristics of the infant BPD population.
Table 2. Characteristics of the infant BPD population.
CharacteristicsNo
BPD
n = 61		Mild
BPD
n = 21		Moderate–Severe
BPD
n = 18
Gestational Age (weeks) ± SD29.1 ± 1.826.1 ± 1.927.1 ± 2.8
Birthweight (grams) ± SD1542 ± 3231109 ± 296803 ± 230
Growth Failure <10% tle n (%)23 (38)4 (19)14 (78)
Growth Failure <3% tle n (%)10 (16)2 (10)6 (33)
Sex—Female n (%)30 (50)14 (67)11 (61)
Sex—Male n (%)31 (50)7 (33)7 (39)
Race and Ethnicity—n (%)
White29 (47)9 (43)8 (44)
Black20 (33)10 (48)7 (39)
Asian/Other/Hispanic12 (20)2 (9)3 (17)
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MDPI and ACS Style

Hendricks-Muñoz, K.D.; Yitayew, M.S.; Chahin, N.; Williams, A.; Xu, J.; Abdulkadir, A.; Alemayehu, B.; Voynow, J.A. The Impact of Enteral Nutrition Type, Volume, and Time of Introduction on the Risk of Growth Failure and Bronchopulmonary Dysplasia in Preterm Infants. Nutrients 2026, 18, 283. https://doi.org/10.3390/nu18020283

AMA Style

Hendricks-Muñoz KD, Yitayew MS, Chahin N, Williams A, Xu J, Abdulkadir A, Alemayehu B, Voynow JA. The Impact of Enteral Nutrition Type, Volume, and Time of Introduction on the Risk of Growth Failure and Bronchopulmonary Dysplasia in Preterm Infants. Nutrients. 2026; 18(2):283. https://doi.org/10.3390/nu18020283

Chicago/Turabian Style

Hendricks-Muñoz, Karen D., Miheret S. Yitayew, Nayef Chahin, Allison Williams, Jie Xu, Adeola Abdulkadir, Bemnet Alemayehu, and Judith A. Voynow. 2026. "The Impact of Enteral Nutrition Type, Volume, and Time of Introduction on the Risk of Growth Failure and Bronchopulmonary Dysplasia in Preterm Infants" Nutrients 18, no. 2: 283. https://doi.org/10.3390/nu18020283

APA Style

Hendricks-Muñoz, K. D., Yitayew, M. S., Chahin, N., Williams, A., Xu, J., Abdulkadir, A., Alemayehu, B., & Voynow, J. A. (2026). The Impact of Enteral Nutrition Type, Volume, and Time of Introduction on the Risk of Growth Failure and Bronchopulmonary Dysplasia in Preterm Infants. Nutrients, 18(2), 283. https://doi.org/10.3390/nu18020283

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