Vitamin E Levels in Preterm and Full-Term Infants: A Systematic Review

Abstract

Vitamin E deficiency (VED) is associated with clinical repercussions in preterm newborns (PTN), but low levels are also found in full-term newborns (TN). As this inadequacy can compromise neurogenesis in childhood, studies are needed to assess whether there is a difference in vitamin E status among newborns according to gestational age to provide support for neonatal monitoring protocols. This systematic review presents a synthesis of the available information on the vitamin E status among PTN and TN. The review was performed according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). Observational studies that evaluated alpha-tocopherol levels were searched in the databases reported in the protocol registered in PROSPERO (CRD42021165152). The Newcastle–Ottawa Scale was used to assess the methodological quality. Overall, 1809 articles were retrieved; 10 were included in the systematic review. In the PTN, the alpha-tocopherol levels ranged from 3.9 to 8.5 mmol/L, while in TN, they were 4.9 to 14.9 mmol/L, and VED ranged from 19% to 100% in newborns. Despite substantial heterogeneity in research methodology and VED classification, the results suggest that the alpha-tocopherol levels among preterm and full-term newborns is below the recommended levels. Our findings demonstrate that further investigations are needed to standardize this classification and to monitor vitamin E status in birth and postnatal with adequate bias control.

Role of Vitamin E in Neonatal Neuroprotection: A Comprehensive Narrative Review

“…Vit E exists in nature as isoforms of tocopherol and tocotrienol. There are alpha (α), beta (β), gamma (γ), and delta (Δ) isoforms of both tocopherol and tocotrienol, resulting in eight total Vit E chemical forms [ 9 , 10 , 11 ]. The most biologically active form is α-tocopherol, which in its natural configuration of D-α-tocopherol (RRR- α-tocopherol) is susceptible to oxidation; therefore, when made synthetically, the phenol group is converted to an ester, making the configuration DL- α-tocopherol (all racemic α-tocopherol), which is more stable [ 9 ].…”

“…Of the other Vit E isoforms, γ-tocopherol is the most abundant in the western diet as it is present in soy and corn oil, but it is not biologically active [ 13 ]. By comparison, α-tocopherol is predominately found in peanut, almond, and sunflower oils, and is dietarily essential [ 11 ]. Humans can absorb all forms of Vit E but cannot interconvert them; therefore, only α-tocopherol is thought to contribute to Vit E demands in humans [ 10 ].…”

“…Vit E has been shown to be involved in implantation, development of the embryo, maturation of the placenta, and protection of the fetus against oxidative stress [ 11 ]. There is low placental transfer of Vit E, though the naturally occurring RRR- α-tocopherol form has been shown to move more readily across the placenta than the racemic α-tocopherol synthetic form [ 47 ].…”

“…Vit E is critical for CNS function beyond the gestational period of development, and its deficiency has been linked to neurodevelopmental delay [ 11 ]. Vit E deficiency in term infants as well as into childhood can lead to progressive neurological disorders, including sensory deficits and hyporeflexia in addition to spinocerebellar ataxia [ 11 , 60 , 61 ]. The above-mentioned anti-oxidative and anti-inflammatory properties of Vit E may provide neuroprotection both postnatally and after hypoxic ischemic injury [ 62 ].…”

“…Vit E is considered safe in preterm and term infants at serum concentrations of 8.5–59 μmol/L (0.5–3.5 mg/L) [ 56 ]. A recent 2022 systematic review found that α-tocopherol levels ranged from 3.9 to 8.5 μmol/L in the preterm infant and 4.9 to 14.9 μmol/L in the term infant [ 11 ]. Although there is no certainty as to what should be considered Vit E deficiency, most studies agree that α-tocopherol levels <12 μmol/L are inadequate.…”