Maternal obesity, child executive functions and child weight gain

母亲肥胖、儿童执行功能和儿童体重增加

• 批准号: 9278240
• 负责人: Bernard F Fuemmeler
• 金额: $ 61.41万
• 依托单位: DUKE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2015
• 资助国家: 美国
• 起止时间: 2015-08-01 至 2020-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9278240
• 关键词: 4 year old; 6 year old; Address; Affect; Affective; Appetite Regulation; Attention; Behavior; Biological; Biological Assay; Birth; Blood; Blood specimen; Body Weight decreased; Body mass index; Brain; Child; Childbirth; Childhood; Cognitive; County; Data; Decision Making; Desire for food; Development; Dietary intake; Distal; Eating; Eating Behavior; Exercise; First Pregnancy Trimester; Future; Goals; Growth; Health; Individual Differences; Knowledge; Laboratories; Lead; Life Style; Link; Mediating; Medical Records; Memory; Metabolic; Metabolism; Modeling; Monocyte Chemoattractant Protein-1; Mothers; Neurocognitive; Obesity; Outcome; Performance; Perinatal; Pregnancy; Pregnancy Complications; Prevention; Prevention program; Prevention strategy; Preventive Intervention; Process; Prospective Studies; Public Health; Recruitment Activity; Research; Risk; Risk Factors; Self-control as a personality trait; Shapes; Short-Term Memory; Stress; Surveys; Umbilical Cord Blood; Visit; Weight; Weight Gain; Woman; base; cohort; cost effective; cytokine; delivery complications; early childhood; eating in absence of hunger; effective therapy; executive function; gestational weight gain; hedonic; improved; inattention; individualized prevention; infancy; maternal obesity; neurodevelopment; neuroinflammation; nutrition; obesity in children; obesity risk; offspring; postnatal; prenatal; prepregnancy obesity; prospective; public health relevance; success

 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.

 描述（由适用提供）：本项目旨在评估儿童肥胖模型，该模型始于母亲怀孕肥胖，是远端风险因素 食欲失调和执行功能不佳的发展，增加了儿童体重增加的风险。这项研究将利用超过2000个出生的围产期出生队列，该研究已从婴儿期到婴儿期获得了前瞻性收集的数据，包括在第一次产前访问时怀孕前体重，妊娠体重增加，妊娠体重增加，对营养行为的关注，压力和生活方式行为，从病历和临床中进行临时及其临时的血液中的数据。拟议的研究将从该队列中招募母亲/儿童二元组，并对智商，执行功能（注意，抑制性控制，记忆力，基于情感的决策做出）进行详细评估，使用食欲调节，在没有饥饿实验室范式，饮食范式，饮食范围和400名儿童的饥饿实验室范式中，在4000名年龄和两年之后的年龄段的400名儿童中饮食。孕期收集的产妇血液标本将用于主张白细胞介核-6（IL-6）和单核细胞化学吸收剂蛋白1（MCP-1），两种在代谢和正常脑发育中都很重要的细胞因子。主要的假设是，孕产妇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。次要/探索性假设是，产前神经炎症过程的标志物介导了孕产妇肥胖对不良儿童结局的影响。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。该研究将有助于解散孕产妇孕前肥胖，儿童食欲调节，执行功能和儿童体重增加之间的关联。通过了解开发人员的因素如何塑造预测儿童对象的个体差异，可以通过针对早期发育时期儿童对象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，以将儿童的体重轨迹转移到更健康的结果。