Depressive symptoms in youth may be a risk factor for obesity, with altered eating behaviors as one possible mechanism. We tested whether depressive symptoms were associated with observed eating patterns expected to promote excessive weight gain in two separate samples. In Study 1, 228 non-treatment-seeking youth, ages 12–17y (15.3 ± 1.4y; 54.7% female), self-reported depressive symptoms using the Beck Depression Inventory. Energy intake was measured as consumption from a 10,934-kcal buffet meal served at 11:00am after an overnight fast. In Study 2, 204 non-treatment-seeking youth, ages 8–17y (13.0 ± 2.8; 49.5% female), self-reported depressive symptoms using the Children’s Depression Inventory. Energy intake was measured as consumption from a 9,835-kcal buffet meal served at 2:30pm after a standard breakfast. In Study 1, controlling for body composition and other relevant covariates, depressive symptoms were positively related to total energy intake in girls and boys. In Study 2, adjusting for the same covariates, depressive symptoms among girls only were positively associated with total energy intake. Youth high in depressive symptoms and dietary restraint consumed the most energy from sweets. In both studies, the effects of depressive symptoms on intake were small. Nevertheless, depressive symptoms were associated with significantly greater consumption of total energy and energy from sweet snack foods, which, over time, could be anticipated to promote excess weight gain.
SUMMARY Brain-derived neurotrophic factor (BDNF) plays a key role in energy balance. In population studies, single nucleotide polymorphisms (SNPs) of the BDNF locus have been linked with obesity, but the mechanism by which these variants cause weight gain is unknown. Here, we examined human hypothalamic BDNF expression in association with 44 BDNF SNPs. We discovered that the minor C allele of rs12291063 is associated with lower human ventromedial hypothalamic BDNF expression (p<0.001) and greater adiposity in both adult and pediatric cohorts (p’s<0.05). We further demonstrated that the major T allele for rs12291063 possesses a binding capacity for the transcriptional regulator, heterogeneous nuclear ribonucleoprotein D0B, knockdown of which disrupts transactivation by the T allele. Binding and transactivation functions are both disrupted by substituting C for T. These findings provide a rationale for BDNF augmentation as a targeted treatment for obesity in individuals who have the rs12291063 CC genotype.
Objective We investigated the manifestations of pediatric loss of control (LOC) eating at different stages of pubertal development. Methods Participants were a non-clinical sample of 468 youth (8–17y). Physical examination determined pubertal stage. LOC eating and disordered eating attitudes were assessed with the Eating Disorder Examination. In a randomized crossover design, a subset (n=244) ate ad libitum from two test meals designed to capture normal and LOC eating. Results There were no differences in the prevalence rates or frequency of reported LOC eating episodes across pubertal stages (ps≥.50). There were, however, puberty by LOC eating interactions in disordered eating attitudes and palatable food consumption (ps≤.05), even after adjusting for age and body composition. LOC eating was associated with elevated global disordered eating attitudes, weight concern, and shape concern in post-pubertal youth (ps≤.001), but not pre-pubertal youth (ps≥.49). In late-puberty, youth with LOC eating consumed less energy from protein (p<.001) and more from carbohydrate (p=.003) and snack-type foods (p=.02) than those without LOC eating, whereas endorsement of LOC eating in pre- or early-to-mid-puberty was not associated with differences in eating behavior (ps≥.20). Conclusions Findings suggest that puberty may be a critical risk period, when LOC eating behaviors in boys and girls may become accompanied by greater weight and shape concerns and more obesogenic food consumption patterns. Interventions for LOC eating during pre-puberty should be evaluated to determine if they are particularly beneficial for the prevention of exacerbated eating disorder psychopathology and adverse weight outcomes.
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