Background

Telomere biology, even during fetal development, is influenced by parental manifestations that can imprint parental epigenetic marks onto the newborn. The interplay between genes, immune biology, and oxidative stress contributes to age-related non-communicable diseases (NCDs), and the telomere length (TL) dynamics in utero are not fully known. This study investigated the impact of parental biomedical factors, including NCDs, on newborn TL, as well as telomerase genes and immune biology.

Method
Blood samples (n=612) were collected from 204 parent–newborn pairs. Their demographics, socioeconomic status (SES), education, and NCD exposure were assessed. TL was quantified using the T/S ratio via qPCR; telomerase gene (TERC, TERT) polymorphisms were identified through Sanger sequencing; and immune senescence was analyzed using flow cytometry. Multivariate regression was used to analyze the paternal–newborn LTL associations, with p<0.05 as the significance threshold.

Results
The mean ages of the mothers and fathers were 27±5.12 and 34±6.36 years, respectively. The newborns of parents aged >30 years old had longer TLs (2.31±1.45; p=0.034). A low SES and blue-collar occupations were correlated with a shorter TL in the parent–newborn pairs (1.5±1.14; p<0.05), with higher frequencies of the telomerase CC genotype (TERC: 28%, 41%; TERT: 22%, 37%) compared to those in high-SES and white-collar groups. NCDs and viral pathologies significantly influenced telomere biology (p<0.05). The analysis of immune senescence markers showed decreased CD57+ KLRG1+ expression in the newborn T-cells (2.45±4.34; p<0.05) compared to those of their parents (3.5±5.49; p=0.04).

Conclusion
Parental biomedical factors and diseases influence newborn telomere biology and immune development in utero, highlighting the importance of mitigating prenatal risk factors.