Evidence for gene-environment correlation in child feeding: Links between common genetic variation for BMI in children and parental feeding practices

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’ (r _A = 0.28 [0.23–0.32]), and substantial and negative between BMI-SDS and ‘pressure’ (r _A = -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.

Author summary

It is widely believed that parents influence their child’s BMI via certain feeding practices. For example, rigid restriction has been argued to cause overweight, and pressuring to eat to cause underweight. However, recent longitudinal research has not supported this model. An alternative hypothesis is that child BMI, which has a strong genetic basis, evokes parental feeding practices (‘gene-environment correlation’). To test this, we applied two genetic methods in a large sample of 10-year-old children from the Twins Early Development Study: a polygenic score analysis (DNA-based score of common genetic variants associated with BMI in genome-wide meta-analyses), and a twin analysis (comparing resemblance between identical and non-identical twin pairs). Polygenic scores correlated positively with parental restriction of food intake (‘restriction’; β = 0.05, p = 4.19x10 ^-4), and negatively with parental pressure to increase food intake (‘pressure’; β = -0.08, p = 2.70x10 ^-7). Associations were unchanged after controlling for all genetic and environmental effects shared within families. Results from twin analyses were consistent. ‘Restriction’ (43%) and ‘pressure’ (54%) were substantially heritable, and a positive genetic correlation between child BMI and ‘restriction’ ( r _A = 0.28), and negative genetic correlation between child BMI and ‘pressure’ ( r _A = -0.48) emerged. These findings challenge the prevailing view that parental behaviours are the sole cause of child BMI by supporting an alternate hypothesis that child BMI also causes parental feeding behaviour.