Objective Genetic variation in the first intron of FTO (e.g., single‐nucleotide polymorphism [SNP] rs9939609) is strongly associated with adiposity. This effect is thought to be mediated (at least in part) via increasing caloric intake, although the precise molecular genetic mechanisms are not fully understood. Prior pediatric studies of FTO have included youth with overweight and obesity; however, they have not informed whether a genotypic effect on ingestive behavior is present prior to obesity onset. Therefore, this study investigated the association between FTO and caloric intake in children aged 5 to 10 years without obesity (adiposity ≤ 95th percentile). Methods A total of 122 children were genotyped for rs9939609 and ate ad libitum from a laboratory lunch buffet following a standardized breakfast. Linear regressions, adjusting for body mass, were used to examine the association between FTO “dose” (number of copies of SNP rs9939609) and intake variables. Results There was a significant association between FTO and total intake. Each risk allele predicted an additional 64 calories, accounting for 3% of the variance. There were no associations between FTO and macronutrient preference, energy density, or diet variety. Results were influenced by race. Conclusions Results corroborate and extend prior work by showing a dose‐dependent effect on food intake in children without obesity.

Adolescence is a critical period for the emergence of eating disorders, and food insecurity may be related to eating pathology and weight, as evidenced in adults. However, little is known about food insecurity and eating pathology during this developmental period, and associations between food insecurity and body mass index (BMI) are mixed. Therefore, we examined associations between food insecurity and BMI percentile, self-reported eating-related pathology and binge eating, and subgroup differences by race/ethnicity. In a subset, we examined the relationship between food insecurity and real-world hunger, food craving, and loss-of-control eating using ecological momentary assessment (EMA). Fifty-eight adolescents at two sites (clinical sample, n = 38, BMI percentile ≥ 70th; community sample, n = 20, all BMI strata) completed self-report questionnaires. Adolescents were 15.2 ± 2.1 years old, 62% female, 50% Black, 34.5% Hispanic, with BMI percentile = 80.5 ± 25.8 (range 4–99). In the full sample, food insecurity was associated with greater BMI (p < 0.01), higher shape/weight overvaluation (p = 0.04), and greater number of binge eating episodes among those reporting at least one binge episode (p < 0.01), with significant relationships for BMI percentile, shape/weight overvaluation, body dissatisfaction, and binge episode frequency among Hispanic adolescents only (each p < 0.01). As in adults, food insecurity may be a risk factor for eating pathology, particularly for Hispanic teens.

Objective Noncoding alleles of the fat mass and obesity-associated (FTO) gene have been associated with obesity risk, yet the underlying mechanisms remain unknown. Risk allele carriers show alterations in brain structure and function, but previous studies have not disassociated the effects of genotype from those of body mass index (BMI). Methods Differences in brain structure and function were examined in children without obesity grouped by their number of copies (0,1,2) of the FTO obesity-risk single-nucleotide polymorphism (SNP) rs1421085. One hundred five 5- to 10-year-olds (5th-95th percentile body fat) were eligible to participate. Usable scans were obtained from 93 participants (15 CC [homozygous risk], 31 CT [heterozygous] and 47 TT [homozygous low risk]). Results Homozygous C allele carriers (CCs) showed greater grey matter volume in the cerebellum and temporal fusiform gyrus. CCs also demonstrated increased bilateral cerebellar white matter fibre density and increased resting-state functional connectivity between the bilateral cerebellum and regions in the frontotemporal cortices. Conclusions This is the first study to examine brain structure and function related to FTO alleles in young children not yet manifesting obesity. This study lends support to the notion that the cerebellum may be involved in FTO-related risk for obesity, yet replication and further longitudinal study are required.

Background: Loss-of-control (LOC) eating commonly develops during adolescence, and it predicts full-syndrome eating disorders and excess weight gain. Although negative emotions and emotion dysregulation are hypothesized to precede and predict LOC eating, they are rarely examined outside the self-report domain. Autonomic indices, including heart rate (HR) and heart rate variability (HRV), may provide information about stress and capacity for emotion regulation in response to stress.Methods: We studied whether autonomic indices predict LOC eating in real-time in adolescents with LOC eating and body mass index (BMI) ⩾70th percentile. Twenty-four adolescents aged 12–18 (67% female; BMI percentile mean ± standard deviation = 92.6 ± 9.4) who reported at least twice-monthly LOC episodes wore biosensors to monitor HR, HRV, and physical activity for 1 week. They reported their degree of LOC after all eating episodes on a visual analog scale (0–100) using a smartphone.Results: Adjusting for physical activity and time of day, higher HR and lower HRV predicted higher self-reported LOC after eating. Parsing between- and within-subjects effects, there was a significant, positive, within-subjects association between pre-meal HR and post-meal LOC rating. However, there was no significant within-subjects effect for HRV, nor were there between-subjects effects for either electrophysiologic variable.Conclusions: Findings suggest that autonomic indices may either be a marker of risk for subsequent LOC eating or contribute to LOC eating. Linking physiological markers with behavior in the natural environment can improve knowledge of illness mechanisms and provide new avenues for intervention.