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.