Friday, April 19, 2024
4/19/2024
PROJECT SUMMARY: As demonstrated by a growing number of studies, stress experienced during pregnancy can lead to significant long-term health problems for mothers and their infants. One biological mechanism that has been identified in heightening a woman’s risk for developing stress-related health complications during pregnancy is the stress hormone cortisol. Further, certain genetic factors, such as the short allele of the (serotonin transporter) 5-HTTLPR gene, have been implicated in increasing one’s cortisol response to stressors in the environment. The impact of these two biomarkers of stress is highly significant in fetal development, as maternal cortisol readily crosses the placenta, potentially causing the fetus to become overly sensitive to environmental stressors after childbirth. Indeed, some studies have shown early life stressors (e.g., socioeconomic adversity, harsh parenting) to accelerate the shortening of telomeres (DNA segments that measure disease risk and biological aging) in children. Yet, few studies have identified pre- and postnatal determinants of infant telomere length among low-income, chronically stressed families. The objective of the proposed study is to prospectively examine whether prenatal maternal and fetal cortisol levels and the 5- HTTLPR genotype of low-income pregnant mothers are predictive of changes in infant telomere length over the first six months postpartum and whether certain maternal and infant characteristics (e.g., exposure to chronic stressors, maternal sensitivity towards their infants) influence these outcomes. A total of 125 low-income mothers will be recruited during pregnancy to provide saliva samples that assess their prenatal cortisol levels and 5-HTTLPR genotype. Mothers will also collect their infant’s hair (within one week after birth) to assess fetal cortisol levels, as well as their infant’s saliva to assess for changes in telomere length from birth to six months postpartum. It is hypothesized that heightened prenatal maternal and fetal cortisol levels and the short allele 5-HTTLPR genotype in mothers will be associated with accelerated shortening of infant telomere length from birth to six months postpartum, and that telomere length will be moderated by certain maternal and infant characteristics (e.g., greater maternal exposure to chronic stressors, less maternal sensitivity towards their infant’s needs). This hypothesis has been formulated from preliminary data collected by the principal investigator and study collaborators. The results of the proposed work have substantial public health implications in advancing our understanding of how prenatal biological mechanisms contribute to the intergenerational transmission of stress outcomes among low-income pregnant mothers and their infants that can have lifelong consequences for the offspring’s health and disease risk. Such findings will also help to identify potential avenues for prevention and treatment, during critical periods of development, to optimize health outcomes for mothers, their children, and subsequent generations.
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