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Scoping Review of Early Toxic Stress and Epigenetic Alterations in the Neonatal Intensive Care Unit
Insights
Early toxic stress in the neonatal intensive care unit (NICU) may alter preterm infants' epigenetics, impacting neurodevelopmental outcomes. Further research is needed to understand these epigenetic alterations and develop interventions.
Area of Science:
- Neonatal intensive care
- Developmental neuroscience
- Epigenetics
Background:
- Preterm infants in the NICU are vulnerable to toxic stress, increasing risks for poor neurodevelopmental outcomes.
- Biological mechanisms linking NICU toxic stress to neurodevelopmental variations in preterm infants are not fully understood.
- Behavioral epigenetics offers a framework for understanding how early stress may cause epigenetic changes affecting infant outcomes.
Purpose of the Study:
- To review the relationship between early toxic stress in the NICU and epigenetic alterations in preterm infants.
- To examine the measurement of early toxic stress exposure and its effects on neurodevelopmental outcomes.
- To explore the role of specific genes in mediating these effects.
Main Methods:
- A scoping review of literature published between 2011 and 2021.
- Searched databases including PubMed, CINAHL, Cochrane Library, PsycINFO, and Web of Science.
- Included primary research on epigenetics, stress, and preterm infants in the NICU.
Main Results:
- Thirteen articles from nine studies were analyzed.
- DNA methylation of six genes (SLC6A4, SLC6A3, OPRMI, NR3C1, HSD11B2, PLAGL1) involved in regulating serotonin, dopamine, and cortisol was studied.
- Alterations in SLC6A4, NR3C1, and HSD11B2 DNA methylation were linked to poorer neurodevelopmental outcomes. NICU stress exposure measurements were inconsistent.
Conclusions:
- Epigenetic changes from NICU toxic stress may influence preterm infants' future neurodevelopmental outcomes.
- Standardized methods for measuring toxic stress exposure in preterm infants are necessary.
- Identifying the epigenome and mechanisms of stress-induced alterations can inform individualized interventions.
Background:
Preterm infants are uniquely vulnerable to early toxic stress exposure while in the neonatal intensive care unit (NICU) and also being at risk for suboptimal neurodevelopmental outcomes. However, the complex biological mechanisms responsible for variations in preterm infants' neurodevelopmental outcomes because of early toxic stress exposure in the NICU remain unknown. Innovative preterm behavioral epigenetics research offers a possible mechanism and describes how early toxic stress exposure may lead to epigenetic alterations, potentially affecting short- and long-term outcomes.
Objective:
The aim of this study was to review the relationships between early toxic stress exposures in the NICU and epigenetic alterations in preterm infants. The measurement of early toxic stress exposure in the NICU and effect of epigenetic alterations on neurodevelopmental outcomes in preterm infants were also examined.
Methods:
We conducted a scoping review of the literature published between January 2011 and December 2021 using databases PubMed, CINAHL, Cochrance Library, PsycINFO, and Web of Science. Primary data-based research that examined epigenetics, stress, and preterm infants or NICU were included.
Results:
A total of 13 articles from nine studies were included. DNA methylations of six specific genes were studied in relation to early toxic stress exposure in the NICU: SLC6A4, SLC6A3, OPRMI, NR3C1, HSD11B2, and PLAGL1. These genes are responsible for regulating serotonin, dopamine, and cortisol. Poorer neurodevelopmental outcomes were associated with alterations in DNA methylation of SLC6A4, NR3C1, and HSD11B2. Measurements of early toxic stress exposure in the NICU were inconsistent among the studies.
Discussion:
Epigenetic alterations secondary to early toxic stress exposures in the NICU may be associated with future neurodevelopmental outcomes in preterm infants. Common data elements of toxic stress exposure in preterm infants are needed. Identification of the epigenome and mechanisms by which early toxic stress exposure leads to epigenetic alterations in this vulnerable population will provide evidence to design and test individualized intervention.
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