Depressive symptoms and observed eating in youth

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 nontreatment- seeking youth, ages 12–17 y (15.3 ± 1.4 y; 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 11:00 am after an overnight fast. In Study 2, 204 non-treatment-seeking youth, ages 8–17 y (13.0 ± 2.8 y; 49.5% female), self-reported depressive symptoms using the Children’s Depression Inventory. Energy intake was measured as consumption from a 9835-kcal buffet meal served at 2:30 pm 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

Human Obesity Associated with an Intronic SNP in the Brain-Derived Neurotrophic Factor Locus

Brain-derived neurotrophic factor (BDNF) plays a key role in energy balance. In population studies, SNPs of the BDNF locus have been linked to 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 observed 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 values < 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

Human obesity associated with an intronic SNP in the brain-derived neurotrophic factor locus

Brain-derived neurotrophic factor (BDNF) plays a key role in energy balance. In population studies, SNPs of the BDNF locus have been linked to 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 observed 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 values < 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