Intergenerational Effects of Stress among Low-Income Pregnant Mothers & their Infants

项目摘要：越来越多的研究表明， 怀孕期间的经历可能会导致严重的长期健康问题， 母亲和他们的婴儿。一种生物学机制已被确定， 增加妇女在怀孕期间患上与压力有关的健康并发症的风险 怀孕是压力荷尔蒙皮质醇。此外，某些遗传因素，如 5-羟色胺转运蛋白基因的短等位基因，与 增加皮质醇对环境中压力的反应。实体就雇员 压力的两个生物标志物在胎儿发育中非常重要， 很容易穿过胎盘，可能导致胎儿对 分娩后的环境压力事实上，一些研究表明， 应激源（例如，社会经济逆境，严厉的养育），以加速缩短 端粒（测量疾病风险和生物衰老的DNA片段）。 然而，很少有研究确定了婴儿端粒长度的产前和产后决定因素 在低收入、长期压力大的家庭中。拟议研究的目的是 前瞻性地检查产前母亲和胎儿的皮质醇水平和5- 低收入孕妇HTTLPR基因型可预测婴儿的变化 端粒长度在产后的前六个月，以及某些母亲和 婴儿特征（例如，暴露于慢性压力源，母亲对 他们的婴儿）影响这些结果。共将招募125名低收入母亲 在怀孕期间提供唾液样本，以评估其产前皮质醇水平， 5-HTTLPR基因型。母亲们也会收集婴儿的头发（在婴儿出生后一周内）。 出生），以评估胎儿皮质醇水平，以及他们的婴儿的唾液，以评估变化 从出生到产后六个月的端粒长度。据推测， 产前母亲和胎儿皮质醇水平和短等位基因5-HTTLPR基因型， 母亲将与婴儿端粒长度从出生起加速缩短有关 到产后六个月，端粒长度将受到某些母亲的调节， 和婴儿特征（例如，更多的母亲暴露于慢性压力源，更少 母亲对婴儿需求的敏感性）。这一假设已经形成 来自主要研究者和研究合作者收集的初步数据。的 建议工作的结果对促进我们的 了解产前生物学机制如何有助于代际 低收入孕妇及其婴儿的压力结果的传播 对后代的健康和疾病风险产生终身影响。等 研究结果还将有助于确定预防和治疗的潜在途径， 发展的关键时期，以优化母亲及其子女的健康成果， 和后代。

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.