Infant's DNA Methylation Age at Birth and Epigenetic Aging Accelerators

Area of Science:

• Epigenetics
• Neonatal Health
• Aging Research

Background:

• Quantifying neonatal biological age is crucial for assessing infant health and maturity.
• A lack of reliable biomarkers currently hinders accurate measurement of biological age in newborns.
• Understanding factors influencing prenatal aging rates is essential for early health interventions.

Purpose of the Study:

• To quantify and assess variability in biological age at birth using a novel epigenetic biomarker.
• To investigate the influence of intrauterine exposures on prenatal aging rates.
• To explore the relationship between maternal factors, race, sex, and neonatal biological age.

Main Methods:

• Utilized a novel epigenetic clock (DNA methylation) to determine methylation age at birth.
• Analyzed cord blood for cell abundance measures and lymphocyte subpopulations.
• Employed partial correlation analysis to assess relationships between maternal socioeconomic status and infant methylation age.
• Investigated the association between prenatal tobacco smoke exposure and accelerated aging.

Main Results:

• Neonatal methylation age was independent of infant sex but significantly influenced by race.
• Lower maternal socioeconomic status was negatively correlated with infant methylation age (r = -0.48, P = 0.005).
• Prenatal tobacco smoke exposure was associated with an increased risk of fast aging (OR = 3.17).
• Tobacco-exposed infants showed altered T cell compartments, including a loss of naive T cells.

Conclusions:

• Common perinatal exposures, such as maternal smoking and lower socioeconomic status, act as significant aging accelerators in neonates.
• The observed loss of naive T cells in infants exposed to tobacco smoke may contribute to smoking-related accelerated aging.
• This study provides the first evidence linking specific perinatal exposures to accelerated biological aging in newborns, highlighting potential targets for intervention.