Abstract

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.

Highlights

  • The home and family environment has been studied for decades with the assumption that it is a crucial determinant of children’s health and development

  • Since the onset of the childhood obesity crisis at the turn of the century, the spotlight has turned onto environmental factors associated with variation in adiposity, in the hope that modifiable elements may be identified as intervention targets

  • In our sample of unrelated individuals, child body mass index (BMI) Genome-wide polygenic score (GPS) was positively correlated with child BMI standard deviation scores (BMI-SDS) (β = 0.20, t(4226) = 13.08, p = 2.41x10-38, R2 = 0.039)

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Summary

Introduction

The home and family environment has been studied for decades with the assumption that it is a crucial determinant of children’s health and development. Parental behaviours have received a great deal of attention. Parents are widely considered to be the ‘gatekeepers’ to their children’s food, and powerful shapers of their developing eating behaviour[1,2,3]. Two types of parental feeding practices (PFPs) in particular have been hypothesised to play a causal role in children’s ability to develop good self-regulation of food intake and determine their weight. Excessive restriction of the type and amount of food a child is allowed to eat (‘restriction’) has been hypothesised to lead to overeating when parental restriction is no longer in place, because the child will potentially hanker after the foods he or she is not usually allowed to eat–the socalled ‘forbidden fruit effect’[1,4,5]. Overly pressuring a child to eat, or to finish everything on the plate (‘pressure’), is thought to be anxiety-provoking for a child with a poor appetite, and serves only to increase undereating further, and compromise weight gain [6,7]

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