Intergenerational transmission of appetite: Associations between mother-child dyads in a Mexican population.

The Child Eating Behaviour Questionnaire (CEBQ) and the Adult Eating Behaviour Questionnaire (AEBQ) measure 'food approach' [Food responsiveness (FR); Emotional overeating (EOE); Enjoyment of food (EF); Desire to Drink] and 'food avoidant' [Satiety responsiveness (SR); Emotional undereating (EUE); Food fussiness (FF); Slowness in eating (SE)] appetitive traits (ATs) in children and adults, respectively. 'Food approach' traits predispose to overweight while 'food avoidance' traits provide protection, but little is known about the relationships between parents' and their offspring's ATs. The aim was to examine the associations between maternal and child appetitive traits, using the AEBQ-Esp and CEBQ-Mex adapted for use in Mexican populations. Sociodemographic data, weights and heights of mothers and their children (aged 3-13 years), who were recruited from a teaching hospital in Guadalajara, Mexico, were measured. Mothers completed both the AEBQ-Esp and the CEBQ-Mex. The CEBQ-Mex was developed, and its reliability was tested using Cronbach's alpha and Omega, and Confirmatory Factor Analysis (CFA) was used to assess its validity. Pearson's correlation coefficients were used to assess associations between mothers' and children's Ats. The sample included 842 mother-child dyads (mother's mean age = 34.8±SD6.9 years, BMI 29.7±6.1 kg/m2; children's mean age = 8.5 ±SD2.5 years, BMIz 1.5±1.6). Internal reliability was moderate to high [Cronbach alpha = .68-.86; Omega = .71-.87] for the CEBQ-Mex and validity was confirmed for an 8-factor model through CFA [RMSEA = 0.065; CFI = 0.840, NFI = 0.805; IFI = 0.842; and χ2(df = 532) = 2939.51, p < 0.001]. All but one of the children's appetitive traits showed small to moderate, significant correlations with their mother's counterpart [FR (r = .22; p<001); EOE (r = .30; p < .001); EF (r = .15; < .001); SR (r = .16; p < .001); EUE (r = .34; p < .001) and FF (r = .14; p < .001). Only SE was not significantly associated with maternal SE (r = .01; p>.05). ATs tend to run in families, signalling the intergenerational transmission of eating behaviours. These may be useful targets for family-wide interventions to support the development and maintenance of healthy eating behaviours in childhood.

Satiety mechanisms in genetic risk of obesity.

IMPORTANCE: A better understanding of the cause of obesity is a clinical priority. Obesity is highly heritable, and specific genes are being identified. Discovering the mechanisms through which obesity-related genes influence weight would help pinpoint novel targets for intervention. One potential mechanism is satiety responsiveness. Lack of satiety characterizes many monogenic obesity disorders, and lower satiety responsiveness is linked with weight gain in population samples. OBJECTIVE: To test the hypothesis that satiety responsiveness is an intermediate behavioral phenotype associated with genetic predisposition to obesity in children. DESIGN, SETTING, AND PARTICIPANTS: Cross-sectional observational study of a population-based cohort of twins born January 1, 1994, to December 31, 1996 (Twins Early Development Study). Participants included 2258 unrelated children (53.3% female; mean [SD] age, 9.9 [0.8] years), one randomly selected from each twin pair. EXPOSURE: Genetic predisposition to obesity. We created a polygenic risk score (PRS) comprising 28 common obesity-related single-nucleotide polymorphisms identified in a meta-analysis of obesity-related genome-wide association studies. MAIN OUTCOMES AND MEASURES: Satiety responsiveness was indexed with a standard psychometric scale (Child Eating Behavior Questionnaire). Using 1990 United Kingdom reference data, body mass index SD scores and waist SD scores were calculated from parent-reported anthropometric data for each child. Information on satiety responsiveness, anthropometrics, and genotype was available for 2258 children. We examined associations among the PRS, adiposity, and satiety responsiveness. RESULTS: The PRS was negatively related to satiety responsiveness (ß coefficient, -0.060; 95% CI, -0.019 to -0.101) and positively related to adiposity (ß coefficient, 0.177; 95% CI, 0.136-0.218 for body mass index SD scores and ß coefficient, 0.167; 95% CI, 0.126-0.208 for waist SD scores). More children in the top 25% of the PRS were overweight than in the lowest 25% (18.5% vs 7.2%; odds ratio, 2.90; 95% CI, 1.98-4.25). Associations between the PRS and adiposity were significantly mediated by satiety responsiveness (P = .006 for body mass index SD scores and P = .005 for waist SD scores). CONCLUSIONS AND RELEVANCE: These results support the hypothesis that low satiety responsiveness is one of the mechanisms through which genetic predisposition leads to weight gain in an environment rich with food. Strategies to enhance satiety responsiveness could help prevent weight gain in genetically at-risk children.