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An FTO Gene Variant Moderates the Association between Parental Restriction and Child BMI.

ABSTRACT: OBJECTIVE:This study aimed to explore whether a common variant in the FTO gene moderates the relationship between parental restriction and child BMI. METHODS:This study reports on baseline data from 178 parent-child (ages 9-10 years) dyads. Parents completed the Child Feeding Questionnaire and reported on socio-demographic characteristics. Each child's height, weight and FTO rs9939609 genotype was assessed. Ordinary least squares regression was used to fit the child's BMI-percentile on parental restriction and the child's FTO genotype, adjusted for covariates. A likelihood ratio test was used to compare a model with and without a multiplicative interaction term between restriction and genotype. RESULTS:Most participants (93.3%) were white, non-Hispanic. Twenty-three percent of children were overweight/obese and FTO genotype was associated with weight status. Mean parental restriction was statistically higher among overweight/obese vs. normal weight children: 3.3 (SD 0.8) vs. 2.8 (SD 1.0); t-test p-value = 0.002. Parental restriction was positively associated with child BMI-percentile and BMI-z only among children with two copies of the high-risk FTO allele (p for interaction = 0.02), where each one-point increase in parental restriction was associated with a 14.7 increase in the child's BMI-percentile or a 0.56-point increase in the child's BMI z-score. CONCLUSION:For only the children with two high-risk alleles, parental restriction was positively associated with child BMI-percentile.

SUBMITTER: Tovar A

PROVIDER: S-EPMC4873182 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

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An FTO Gene Variant Moderates the Association between Parental Restriction and Child BMI.

Tovar Alison A Emond Jennifer A JA Hennessy Erin E Gilbert-Diamond Diane D

PloS one 20160519 5

<h4>Objective</h4>This study aimed to explore whether a common variant in the FTO gene moderates the relationship between parental restriction and child BMI.<h4>Methods</h4>This study reports on baseline data from 178 parent-child (ages 9-10 years) dyads. Parents completed the Child Feeding Questionnaire and reported on socio-demographic characteristics. Each child's height, weight and FTO rs9939609 genotype was assessed. Ordinary least squares regression was used to fit the child's BMI-percenti ...[more]

PMID: 27196523

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Project description:BackgroundIn a longitudinal cohort study, we investigated the interplay of harsh parenting and genetic variation across a set of functionally related dopamine genes, in association with children's externalizing behavior. This is one of the first studies to employ gene-based and gene-set approaches in tests of Gene by Environment (G × E) effects on complex behavior. This approach can offer an important alternative or complement to candidate gene and genome-wide environmental interaction (GWEI) studies in the search for genetic variation underlying individual differences in behavior.MethodsGenetic variants in 12 autosomal dopaminergic genes were available in an ethnically homogenous part of a population-based cohort. Harsh parenting was assessed with maternal (n = 1881) and paternal (n = 1710) reports at age 3. Externalizing behavior was assessed with the Child Behavior Checklist (CBCL) at age 5 (71 ± 3.7 months). We conducted gene-set analyses of the association between variation in dopaminergic genes and externalizing behavior, stratified for harsh parenting.ResultsThe association was statistically significant or approached significance for children without harsh parenting experiences, but was absent in the group with harsh parenting. Similarly, significant associations between single genes and externalizing behavior were only found in the group without harsh parenting. Effect sizes in the groups with and without harsh parenting did not differ significantly. Gene-environment interaction tests were conducted for individual genetic variants, resulting in two significant interaction effects (rs1497023 and rs4922132) after correction for multiple testing.ConclusionOur findings are suggestive of G × E interplay, with associations between dopamine genes and externalizing behavior present in children without harsh parenting, but not in children with harsh parenting experiences. Harsh parenting may overrule the role of genetic factors in externalizing behavior. Gene-based and gene-set analyses offer promising new alternatives to analyses focusing on single candidate polymorphisms when examining the interplay between genetic and environmental factors.

Project description: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 (? = 0.20, p = 2.41x10-38). Consistent with the gene-environment correlation hypothesis, child BMI GPS was positively associated with 'restriction' (? = 0.05, p = 4.19x10-4), and negatively associated with 'pressure' (? = -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.

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An FTO Gene Variant Moderates the Association between Parental Restriction and Child BMI.

Publications

An FTO Gene Variant Moderates the Association between Parental Restriction and Child BMI.

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