Nutritional therapies and BPD
If early and rapid advancement of enteral nutrition relates to a decrease in BPD, what might be the critical nutrient exposure? In a systematic review, Huang et al demonstrated that exclusive and partial human milk diets were associated with lower risk of BPD in preterm infants.(Huang et al. 2019) Patel et al also demonstrated that each 10% increase in mother’s own milk dose was associated with a decreased risk of BPD at 36-week corrected age.(Patel et al. 2017) In the Behnke et al study, in which feedings were initiated on the first postnatal day with standard preterm formula and maternal milk as available, it would be interesting to know the proportion of feeds which were maternal milk.
The specific components of human milk which may protect and/or support lung development include long chain polyunsaturated fatty acids (LC-PUFAs), which promote cell membrane function and surfactant production. Additionally, LC-PUFAs have anti-inflammatory properties, which may have benefits in the repair of neonatal lung injury. Postnatal docosahexaenoic acid (DHA) concentrations were inversely associated with BPD risk in one observational study of infants born < 30 weeks gestational age.(Martin et al. 2011) Randomized trials of maternal and preterm infant DHA and arachidonic acid supplementation are ongoing. (Wendel et al. 2021) Studies specifically examining the role of PUFAs in reducing risk of lung disease in extremely preterm infants are needed.
Vitamins such as vitamin A, or retinoic acid, and vitamin D also have roles in respiratory outcomes.(Onwuneme et al. 2015; Tyson et al. 1999) Intramuscular injections of vitamin A related to a 7% reduction in BPD or death in a clinical trial, but similar benefit is not yet shown with enteral supplementation.(Tyson et al. 1999) Further investigation is needed to identify the specific paths by which enteral nutrients may mitigate BPD progression.