Maternal obesity, child executive functions and child weight gain

 描述(由申请人提供)：本项目旨在评估一种儿童肥胖模型，该模型始于孕妇孕前肥胖，是导致儿童肥胖的一个远端危险因素。 出现食欲失调和执行功能不佳，增加儿童超重的风险。这项研究将利用2000多名新生儿的围产期队列，这些队列获得了从怀孕前三个月到婴儿时期的前瞻性数据，包括第一次产前探视时的孕前体重、妊娠体重增加、关于营养、压力和生活方式行为的调查、关于怀孕和分娩并发症的医疗记录数据、怀孕前三个月的母亲血液和分娩时的脐带血。这项拟议的研究将从这一队列中招募母子二人组，并对400名4岁和2岁后6岁的儿童进行详细的智商、执行功能(注意力、抑制控制、记忆、基于情感的决策)、食欲调节(在没有饥饿的情况下进食)、饮食摄入量和人体发育的评估。在怀孕前三个月收集的母血样本和出生时的脐带血将用于检测白细胞介素6(IL-6)和单核细胞趋化蛋白1(MCP-1)，这两种细胞因子对新陈代谢和正常大脑发育都很重要。主要的假设是，母亲肥胖会影响调节食欲和执行功能的神经发育过程，从而增加后代肥胖的风险。第二个/探索性假设是，产前神经炎症过程的标志物介导了母亲肥胖对儿童不良结局的影响。在已建立的围产期出生队列的背景下进行这项研究，为实现我们的目标提供了一个具有成本效益的机会。这项研究将有助于理清母亲孕前肥胖、儿童食欲调节、执行功能和儿童体重增加之间的关系。通过了解发育因素如何塑造预测儿童肥胖的个体差异，有可能通过在儿童发育早期针对儿童肥胖的关键风险因素来显著改进预防干预措施，并创建量身定制的预防计划，将儿童的体重轨迹转向更健康的结果。

 DESCRIPTION (provided by applicant): This project seeks to evaluate a model of childhood obesity that begins with maternal pre-pregnancy obesity as a distal risk factor contributing to the development of appetite dysregulation and poor executive functioning, increasing a child's risk for excess weight gain. The study will take advantage of a perinatal birth cohort with over 2000 births that has obtained prospectively collected data from the first trimester through infancy, inclusive of pre-pregnancy weight at the first prenatal visit, gestational weight gain, surveys regarding nutrition, stress and lifestyle behaviors, data from medical records on pregnancy and birth complications, maternal blood at the first trimester, and umbilical cord blood at delivery. The proposed study will recruit mother/child dyads from this cohort and conduct detailed assessments of IQ, executive functions (attention, inhibitory control, memory, affective-based decision making), appetite regulation using the eating in the absence of hunger laboratory paradigm, dietary intake, and anthropometric growth among 400 children at ages 4 years and two- years later at 6 years. Maternal blood specimens collected during the first trimester and cord blood at birth will be used to assay Interleuken-6 (IL-6) and monocyte chemoattractant protein 1 (MCP-1), two cytokines important in both metabolism and normal brain development. The primary hypothesis is that maternal obesity influences neurodevelopmental processes that regulate appetite and executive functions resulting in increased risk for obesity in offspring. A secondary/exploratory hypothesis is that markers of prenatal neuro-inflammatory processes mediate the effect of maternal obesity on adverse child outcomes. Conducting this study in the context of an established perinatal birth cohort provides a cost-effective opportunity to achieve our aims. The study will aid in disentangling the associations between maternal pre-pregnancy obesity, childhood appetite regulation, executive functions and child weight gain. By understanding how developmental factors shape individual differences that predict child obesity, it is possible to markedly improve prevention interventions by targeting key risk factors for childhood obesity at earlier developmental periods and create tailored prevention programs that shift children's weight trajectory toward more healthy outcomes.