Institute of Psychiatry, Psychology and Neuroscience, MRC Social, Genetic and Developmental Psychiatry Centre, King's College London, London, United Kingdom.
NIHR Biomedical Research Centre for Mental Health, South London and Maudsley NHS Trust, London, United Kingdom.
PLoS Genet. 2018 Nov 20;14(11):e1007757. doi: 10.1371/journal.pgen.1007757. eCollection 2018 Nov.
The parental feeding practices (PFPs) of excessive restriction of food intake ('restriction') and pressure to increase food consumption ('pressure') have been argued to causally influence child weight in opposite directions (high restriction causing overweight; high pressure causing underweight). However child weight could also 'elicit' PFPs. A novel approach is to investigate gene-environment correlation between child genetic influences on BMI and PFPs. Genome-wide polygenic scores (GPS) combining BMI-associated variants were created for 10,346 children (including 3,320 DZ twin pairs) from the Twins Early Development Study using results from an independent genome-wide association study meta-analysis. Parental 'restriction' and 'pressure' were assessed using the Child Feeding Questionnaire. Child BMI standard deviation scores (BMI-SDS) were calculated from children's height and weight at age 10. Linear regression and fixed family effect models were used to test between- (n = 4,445 individuals) and within-family (n = 2,164 DZ pairs) associations between the GPS and PFPs. In addition, we performed multivariate twin analyses (n = 4,375 twin pairs) to estimate the heritabilities of PFPs and the genetic correlations between BMI-SDS and PFPs. The GPS was correlated with BMI-SDS (β = 0.20, p = 2.41x10-38). Consistent with the gene-environment correlation hypothesis, child BMI GPS was positively associated with 'restriction' (β = 0.05, p = 4.19x10-4), and negatively associated with 'pressure' (β = -0.08, p = 2.70x10-7). These results remained consistent after controlling for parental BMI, and after controlling for overall family contributions (within-family analyses). Heritabilities for 'restriction' (43% [40-47%]) and 'pressure' (54% [50-59%]) were moderate-to-high. Twin-based genetic correlations were moderate and positive between BMI-SDS and 'restriction' (rA = 0.28 [0.23-0.32]), and substantial and negative between BMI-SDS and 'pressure' (rA = -0.48 [-0.52 - -0.44]. Results suggest that the degree to which parents limit or encourage children's food intake is partly influenced by children's genetic predispositions to higher or lower BMI. These findings point to an evocative gene-environment correlation in which heritable characteristics in the child elicit parental feeding behaviour.
父母的喂养方式(PFPs),包括过度限制食物摄入(“限制”)和增加食物消费的压力(“压力”),被认为会以相反的方向对儿童体重产生因果影响(高限制导致超重;高压力导致体重不足)。然而,儿童体重也可能“引发”PFPs。一种新的方法是研究儿童 BMI 遗传影响与 PFPs 之间的基因-环境相关性。使用来自独立全基因组关联研究荟萃分析的结果,为双胞胎早期发展研究中的 10346 名儿童(包括 3320 对 DZ 双胞胎)创建了结合 BMI 相关变异的全基因组多基因评分(GPS)。使用儿童喂养问卷评估父母的“限制”和“压力”。根据儿童在 10 岁时的身高和体重计算 BMI 标准差得分(BMI-SDS)。线性回归和固定家庭效应模型用于测试 GPS 与 PFPs 之间的个体间(n=4445 人)和家庭内(n=2164 DZ 对)关联。此外,我们进行了多元双胞胎分析(n=4375 对双胞胎),以估计 PFPs 的遗传度以及 BMI-SDS 与 PFPs 之间的遗传相关性。GPS 与 BMI-SDS 相关(β=0.20,p=2.41x10-38)。与基因-环境相关性假设一致,儿童 BMI GPS 与“限制”呈正相关(β=0.05,p=4.19x10-4),与“压力”呈负相关(β=-0.08,p=2.70x10-7)。在控制了父母 BMI 后,以及在控制了整体家庭贡献(家庭内分析)后,这些结果仍然一致。“限制”(43%[40%-47%])和“压力”(54%[50%-59%])的遗传度为中等到高。基于双胞胎的遗传相关性在 BMI-SDS 和“限制”之间为中度且为正(rA=0.28[0.23-0.32]),在 BMI-SDS 和“压力”之间为实质性且为负(rA=-0.48[-0.52--0.44])。结果表明,父母限制或鼓励儿童进食的程度部分受儿童 BMI 遗传倾向的影响。这些发现表明存在一种唤起的基因-环境相关性,其中儿童的遗传特征会引发父母的喂养行为。