total of 13.7 million children in the United States younger than 18 years are obese, and an additional 12 million children are classified as overweight. 1 The percentage of extreme obesity among children has continued to increase in the past decade and is now estimated to be approximately 750 000, or 6%, of children who meet the diagnostic threshold for obesity. 2 The negative metabolic and cardiovascular sequelae of increasing adiposity, obesity, and chronic obesity in children is well established. Children with obesity are more likely to develop early-onset type 2 diabetes and heart disease, [3][4][5] tend to have more severe risk factors and disease burden, 6 and are at greater risk for premature mortality than their healthy weight peers. 7,8 Higher body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared) has also been associated with poorer cognitive performance across the lifespan, particularly in the domain of higher executive functions. [9][10][11][12] Less is known about the effects of obesity and being overweight on brain development and how this might interact with cognitive ability. Many neuroimaging studies [13][14][15][16] have found structural alterations in cortical regions involved in executive control in obese children compared with lean children. However, limited sample sizes, insufficient statistical power, differences in sample populations, and differing magnetic resonance imaging (MRI) modalities have yielded mixed results. Maayan et al 13 reported that obese children performed worse on working memory tasks compared with healthy control individuals and had less orbitofrontal cortical volume, a brain region associated with appetite control. By contrast, Saute et al 14 found an association between IMPORTANCE A total of 25.7 million children in the United States are classified as overweight or obese. Obesity is associated with deficits in executive function, which may contribute to poor dietary decision-making. Less is known about the associations between being overweight or obese and brain development.OBJECTIVE To examine whether body mass index (BMI) is associated with thickness of the cerebral cortex and whether cortical thickness mediates the association between BMI and executive function in children. DESIGN, SETTING, AND PARTICIPANTSIn this cross-sectional study, cortical thickness maps were derived from T1-weighted structural magnetic resonance images of a large, diverse sample of 9-and 10-year-old children from 21 US sites. List sorting, flanker, matrix reasoning, and Wisconsin card sorting tasks were used to assess executive function. MAIN OUTCOMES AND MEASURESA 10-fold nested cross-validation general linear model was used to assess mean cortical thickness from BMI across cortical brain regions. Associations between BMI and executive function were explored with Pearson partial correlations. Mediation analysis examined whether mean prefrontal cortex thickness mediated the association between BMI and executive function.RESULTS Among 3190 individuals (me...

The prevalence of obesity in children and adolescents worldwide has quadrupled since 1975 and is a key predictor of obesity later in life. Previous work has consistently observed relationships between macroscale measures of reward-related brain regions (e.g., the nucleus accumbens [NAcc]) and unhealthy eating behaviors and outcomes; however, the mechanisms underlying these associations remain unclear. Recent work has highlighted a potential role of neuroinflammation in the NAcc in animal models of diet-induced obesity. Here, we leverage a diffusion MRI technique, restriction spectrum imaging, to probe the microstructure (cellular density) of subcortical brain regions. More specifically, we test the hypothesis that the cell density of reward-related regions is associated with obesity-related metrics and early weight gain. In a large cohort of nine- and ten-year-olds enrolled in the Adolescent Brain Cognitive Development (ABCD) study, we demonstrate that cellular density in the NAcc is related to individual differences in waist circumference at baseline and is predictive of increases in waist circumference after 1 y. These findings suggest a neurobiological mechanism for pediatric obesity consistent with rodent work showing that high saturated fat diets increase gliosis and neuroinflammation in reward-related brain regions, which in turn lead to further unhealthy eating and obesity.

Highlights BMI was associated with widespread structural differences in cortical thickness, surface area, subcortical gray matter volumes and in white matter estimates of fractional anisotropy and mean diffusivity. BMI was also associated with altered resting-state functional connectivity and working memory during an EN-back task but, contrary to some extant findings, was not related to reward or inhibitory control (as assessed by the Monetary Incentive Delay task and Stop Signal Task). Excessive weight gain (i.e., more than 20 pounds in a year) was associated at baseline with thicker cortices, and differences in surface area and white matter in regions associated with attention and appetite control (e.g., insula, parahippocampal gyrus), but no functional associations were observed. All analyses quantified generalizability to an unseen test set. These findings suggest that brain structure, resting state and working memory are associated with current weight and that brain structure may have potential as an MRI biomarker to identify children at risk for pathological weight gain.

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Adolescents with food addiction or with a higher number of food addiction symptoms may warrant additional resources to support adherence to and retention with a weight management program. Implementing screening measures for food addiction before enrolling in a weight management program may be an effective strategy to identify adolescents who may benefit from adjunct modalities.