SECONDARY ANALYSES OF RCT DATA ON SENSITIVE PERIODS IN FLAVOR LEARNING AND DIET AMONG BREASTFEEDING DYADS

摘要 简介：我们的目标是评估产后期间饮食的直接和间接影响， 母乳喂养的母婴二人组。除了完成随机对照试验的主要目的外， 一项随机对照试验（RCT）旨在描述母乳中饮食传播的蔬菜风味的影响， 在味道学习的敏感期，我们有一个全面的数据集，重复和多样化的母亲和 在RCT过程中收集的婴儿表型。试验从产后2周开始， 婴儿断奶后开始吃固体食物，并在10.5个月和1岁时进行干预后随访。所以我们 这是一个独特的机会，超越了最初RCT关于高度普遍现象的目标， 母乳喂养和营养方案。 在整个干预和干预后阶段收集的次要结局表型（10.5 月，1年）包括人体测量（从中我们确定体重增加轨迹[g/d]， 二分体两个成员的饮食摄入量;婴儿发育里程碑;脂肪 和母乳的热量含量;以及母亲的喂养方式和目标。我们提出的二次分析 这里将测试几个假设，以比较次要结果与基于实验室的主要结果。 测量婴儿蔬菜接受度、母体蔬菜口味等级和口味基因型。母乳喂养 (BF)在我们的RCT队列中是稳健和持久的，81%的婴儿持续10.5个月或更长时间， 只有三分之一的人喂过婴儿配方奶粉。因此，对于两个目标（AIMS 1，2），我们还将比较从 这一特征良好的BF队列，使用相同的方法收集了纵向队列的数据， 完全配方奶粉喂养的婴儿和母亲。该提案的核心是四个目标， 完成后将产生至少六份出版物。 AIM 1将使用重复测量的母亲喂养实践和母乳成分的数据来测试 母乳中的脂肪含量和母亲的反应性喂养有助于婴儿 随着时间的推移体重增加的轨迹。因为与FF相比，母乳喂养在1岁时可以防止肥胖 队列中，我们还将确定BF组和FF组之间在母亲喂养方面是否存在差异 随着时间的推移，他们喂养婴儿的补充饮食的类型。AIM 2将确定早期风险 快速增重轨迹和母乳成分等因素相互作用或独立作用， 影响乳牙萌出，一个假设的生物标志物，为以后的肥胖风险。AIM 3将表征 长期以来母亲饮食的营养和能量含量及其与子女饮食的一致性。而 遗传变异并不有助于最初的蔬菜接受，AIM 4将测试假设，TAS 2 R38 基因型解释了干预后饮食措施的变化，因此那些具有不敏感等位基因的人将显示 蔬菜摄入量比那些对食物敏感等位基因纯合子的人多。 从这些二次分析中获得的知识可以转化为行为干预， 促进健康的母亲饮食和喂养做法，从而支持婴儿健康的体重增加和饮食。

ABSTRACT Précis: Our goal is to assess both the direct and indirect effects of diet during the postpartum period in breastfeeding mother-infant dyads. In addition to accomplishing the primary aims of a randomized controlled trial (RCT) designed to characterize the effects of diet-transmitted vegetable flavors in mother’s milk during sensitive period in flavor learning, we have a comprehensive data set of repeated and diverse maternal and infant phenotypes collected during the course of the RCT. The trial lasted from 2 weeks postpartum until the infants were weaned to solid foods, with post-intervention visits at 10.5 months and 1 year. Therefore, we have a unique opportunity that goes beyond the goals of the original RCT on the highly pervasive phenomenon of breastfeeding and nutritional programming. The secondary outcome phenotypes collected throughout the intervention and post-intervention periods (10.5 mos, 1 y) included measures of anthropometry (from which we determined weight gain trajectories [g/d], a risk factor for later obesity) and dietary intake of both members of the dyad; infant developmental milestones; fat and caloric content of breast milk; and maternal feeding styles and goals. The secondary analyses we propose here will test several hypotheses to compare the secondary outcomes with primary outcomes of lab-based measures of infant vegetable acceptance, maternal vegetable taste ratings, and taste genotype. Breastfeeding (BF) was robust and persistent for our RCT cohort, lasting for 10.5 mos or longer for 81% of the infants, and only one-third ever fed infant formula. Thus, for two aims (AIMS 1, 2) we will also compare data collected from this well-characterized BF cohort with data collected using identical methods on a longitudinal cohort of exclusively formula-fed (FF) infants and mothers. At the heart of the proposal are four aims, which upon completion will yield at least six publications. AIM 1 will use data from repeated measures of maternal feeding practices and breast milk composition to test the primary hypothesis that the fat content of breast milk and maternal responsive feeding contributes to infant weight gain trajectories over time. Because breastfeeding protected against obesity at 1 y compared to the FF cohort, we will also determine whether there are differences between BF and FF groups in maternal feeding styles over time and the type of complementary diet they feed their infants. AIM 2 will determine how early risk factors—rapid weight gain trajectories and breast milk composition,—interact together or act independently to influence primary tooth eruption, a hypothesized biomarker for later obesity risk. AIM 3 will characterize nutrient and energy content of the diets of mothers over time and concordance with their children’s diets. While genetic variation did not contribute to initial vegetable acceptance, AIM 4 will test the hypothesis that TAS2R38 genotype explains variation in post-intervention diet measures such that those with insensitive alleles will show greater vegetable intakes than those homozygous for the bitter-sensitive allele. The knowledge gained from these secondary analyses could be translated to behavioral interventions to promote healthy maternal diet and feeding practices that in turn support healthy weight gain and diet in infants.