Background: Body mass index (BMI) has been shown to be highly heritable, but most studies were carried out in cohorts born before the onset of the “obesity epidemic.” Objective: We aimed to quantify genetic and environmental influences on BMI and central adiposity in children growing up during a time of dramatic rises in pediatric obesity. Design: We carried out twin analyses of BMI and waist circumference (WC) in a UK sample of 5092 twin pairs aged 8–11 y. Quantitative genetic model-fitting was used for the univariate analyses, and bivariate quantitative genetic model-fitting was used for the analysis of covariance between BMI and WC. Results: Quantitative genetic model-fitting confirmed substantial heritability for BMI and WC (77% for both). Bivariate genetic analyses showed that, although the genetic influence on WC was largely common to BMI (60%), there was also a significant independent genetic effect (40%). For both BMI and WC, there was a very modest shared-environment effect, and the remaining environmental variance was unshared. Conclusions: Genetic influences on BMI and abdominal adiposity are high in children born since the onset of the pediatric obesity epidemic. Most of the genetic effect on abdominal adiposity is common to BMI, but 40% is attributable to independent genetic influences. Environmental effects are small and are divided approximately equally between shared and nonshared effects. Targeting the family may be vital for obesity prevention in the earliest years, but longer-term weight control will require a combination of individual engagement and society-wide efforts to modify the environment, especially for children at high genetic risk.

Context: Polymorphisms within the FTO gene have consistently been associated with obesity across multiple populations. However, to date, it is not known whether the association between genetic variation in FTO and obesity is mediated through effects on energy intake or energy expenditure. Objective: Our objective was to examine the association between alleles of FTO known to increase obesity risk and measures of habitual appetitive behavior. Methods: The intronic FTO single nucleotide polymorphism (rs9939609) was genotyped in 3337 United Kingdom children in whom measures of habitual appetitive behavior had been assessed using two scales (Satiety Responsiveness and Enjoyment of Food) from the Child Eating Behaviour Questionnaire, a psychometric tool that has been validated against objective measures of food intake. Associations of FTO genotype with indices of adiposity and appetite were assessed by ANOVA. Results: As expected, the A allele was associated with increased adiposity in this cohort and in an independent case-control replication study of United Kingdom children of similar age. AA homozygotes had significantly reduced Satiety Responsiveness scores (P = 0.008, ANOVA). Mediation analysis indicated that the association of the AA genotype with increased adiposity was explained in part through effects on Satiety Responsiveness. Conclusions: We have used a unique dataset to examine the relationship between a validated measure of children’s habitual appetitive behavior and FTO obesity risk genotype and conclude that the commonest known risk allele for obesity is likely to exert at least some of its effects by influencing appetite.