Maternal obesity, child executive functions and child weight gain

 描述（由申请人提供）：该项目旨在评估一个儿童肥胖模型，该模型以母亲孕前肥胖作为导致儿童肥胖的远端风险因素。 食欲失调和执行功能差的发展，增加了儿童体重过度增加的风险。这项研究将利用一个有2000多名新生儿的围产期出生队列，该队列已经获得了从前三个月到婴儿期的前瞻性收集的数据，包括首次产前访视时的孕前体重，妊娠期体重增加，关于营养、压力和生活方式行为的调查，来自妊娠和出生并发症医疗记录的数据，前三个月的母体血液，以及分娩时的脐带血拟议的研究将从该队列中招募母亲/儿童对，并在400名4岁和2年后6岁儿童中使用无饥饿实验室范式进食对智商、执行功能（注意力、抑制控制、记忆、基于情感的决策）、食欲调节、饮食摄入和人体测量生长进行详细评估。在妊娠早期采集的母体血液样本和出生时采集的脐带血样本将用于测定白细胞介素-6（IL-6）和单核细胞趋化蛋白1（MCP-1），这两种细胞因子在代谢和正常脑发育中均很重要。主要假设是母亲肥胖影响调节食欲和执行功能的神经发育过程，导致后代肥胖风险增加。一个次要/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不良儿童结局的影响。在一个既定的围产期出生队列的背景下进行这项研究提供了一个具有成本效益的机会，以实现我们的目标。这项研究将有助于解开母亲孕前肥胖，儿童食欲调节，执行功能和儿童体重增加之间的联系。通过了解发育因素如何塑造预测儿童肥胖的个体差异，可以通过在早期发育阶段针对儿童肥胖的关键风险因素来显着改善预防干预措施，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.