Update on Vitamin E and Its Potential Role in Preventing or Treating Bronchopulmonary Dysplasia

Stone et al, Neonatology, 2018


Vitamin E is obtained only through the diet and has a number of important biological activities, including functioning as an antioxidant. Evidence that free radicals may contribute to pathological processes such as bronchopulmonary dysplasia (BPD), a disease of prematurity associated with increased lung injury, inflammation and oxidative stress, led to trials of the antioxidant vitamin E (α-tocopherol) to prevent BPD with variable results. These trials were all conducted at supraphysiologic doses and 2 of these trials utilized a formulation containing a potentially harmful excipient. Since 1991, when the last of these trials was conducted, both neonatal management strategies for minimizing oxygen and ventilator-related lung injury and our understanding of vitamin E isoforms in respiratory health have advanced substantially. It is now known that there are differences between the effects of vitamin E isoforms α-tocopherol and γ-tocopherol on the development of respiratory morbidity and inflammation. What is not known is whether improvements in physiologic concentrations of individual or combinations of vitamin E isoforms during pregnancy or following preterm birth might prevent or reduce BPD development. The answers to these questions require adequately powered studies targeting pregnant women at risk of preterm birth or their premature infants immediately following birth, especially in certain subgroups that are at increased risk of vitamin E deficiency (e.g., smokers). The objective of this review is to compile, update, and interpret what is known about vitamin E isoforms and BPD since these first studies were conducted, and suggest future research directions.


At present, there is insufficient evidence about the benefits and risks of vitamin E in BPD prevention to make evidence-based recommendations about supplementation. However, new data on the effects of the individual vitamin E isoforms on lung health should make us relook at this essential dietary factor as a potential preventive or treatment intervention for BPD. Adequately powered studies will be needed to address whether supplementation of specific vitamin E isoforms either in pregnant women at risk of preterm birth, or in at-risk premature infants immediately following birth, reduces the development of BPD and subsequent long-term pulmonary morbidity in childhood and adult life.