Concerns have been raised about excessive or “addictive” phone use among adolescents, and the impact that addictive phone use (APU) can have on adolescent development and health. Most research on the physical health correlates of smartphone use has been limited to sleep health, whereas other outcomes, such as eating behaviors and obesity risk have not received as much attention. To address this gap in the literature, we examined the association between APU and emotion regulation difficulties, impulsivity, maladaptive eating behaviors, and adiposity in a sample of 111 adolescents. We found that APU is associated with greater emotion regulation difficulties, dysregulated eating, restrained eating, food addiction, and higher percent body fat. Further, we found that emotion regulation difficulties mediated the association between APU and dysregulated eating, restrained eating, and food addiction. Findings suggest that addictive phone use may confer increased risk for obesogenic eating behaviors and food addiction via challenges in regulating emotions.

Emerging data suggest that weight gain is associated with changes in neural response to palatable food tastes and palatable food cues, which may serve to maintain overeating. We investigated whether weight gain is associated with neural changes in response to tastes of milkshakes varying in fat and sugar content and palatable food images. We compared changes in neural activity between initially healthy-weight adolescents who gained weight (n = 36) and those showing weight stability (n = 31) over 2–3 y. Adolescents who gained weight compared with those who remained weight stable showed decreases in activation in the postcentral gyrus, prefrontal cortex, insula, and anterior cingulate cortex, and increases in activation in the parietal lobe, posterior cingulate cortex, and inferior frontal gyrus in response to a high-fat/low-sugar compared with low-fat/low-sugar milkshake. Weight gainers also showed greater decreases in activation in the anterior insula and lateral orbitofrontal cortex in response to a high-fat/high-sugar compared with low-fat/low-sugar milkshake than those who remained weight stable. No group differences emerged in response to a low-fat/high-sugar compared with a low-fat/low-sugar milkshake. Weight gainers compared with those who remained weight stable showed greater decreases in activation in the middle temporal gyrus and increases in cuneus activation in response to appetizing compared with unappetizing food pictures. The significant interactions were partially driven by group differences in baseline responsivity and by opposite changes in neural activation in adolescents who remained weight stable. Data suggest that weight gain is associated with a decrease in responsivity of regions associated with taste and reward processing to palatable high-fat- and high-fat/high-sugar food tastes. Data also suggest that avoiding weight gain increases taste sensitivity, which may prevent future excessive weight gain. This trial was registered at clinicaltrials.gov as NCT01949636.

Identifying correlates of brain response to food cues and taste provides critical information on individual differences that may influence variability in eating behavior. However, a few studies examine how brain response changes over repeated exposures and the individual factors that are associated with these changes. Using functional magnetic resonance imaging, we examined how brain response to a palatable taste and proceeding cues changed over repeated exposures and how individual differences in weight, familial obesity risk, dietary restraint and reward responsiveness correlate with these changes. In healthy-weight adolescents (n = 154), caudate and posterior cingulate cortex (PCC) response increased with repeated cue presentations, and oral somatosensory cortex and insula response increased with repeated milkshake tastes. The magnitude of increase over exposures in the left PCC to cues was positively associated with body mass index percentile (r = 0.18, P = 0.026) and negatively associated with dietary restraint scores (r = −0.24, P = 0.003). Adolescents with familial obesity risk showed higher cue-evoked caudate response across time, compared to the low-risk group (r = 0.12, P = 0.035). Reward responsiveness positively correlated with right oral somatosensory cortex/insula response to milkshake over time (r = 0.19, P = 0.018). The results show that neural responses to food cues and taste change over time and that individual differences related to weight gain are correlated with these changes.

Objective: To test whether overweight/obesity is associated with an elevated reward region response to milkshake cues and a low reward region response to milkshake receipt. To test whether the risk for eating pathology moderates the effects of weight status on the neural response to milkshake cues and milkshake receipt. Method: The current study used functional magnetic resonance imaging (fMRI) to examine the neuronal responses of female adolescents (n = 80; M age = 14.6 ± 0.9; M BMI = 21.9 ± 3.6; 41% with a biological parental history of eating pathology) during a food receipt paradigm. Results: Females with overweight/obesity showed a greater ventromedial prefrontal cortex (vmPFC), and ventral anterior cingulate (ACC) response to milkshake cues and a greater ventral striatum, subgenual ACC, and dorsomedial prefrontal cortex response to milkshake receipt than those with a healthy weight. Females with overweight/obesity plus a parental history of eating pathology showed a greater vmPFC/medial orbitofrontal cortex response to milkshake cues than those without a parental history of eating pathology and those with a healthy weight. Females with overweight/obesity and without a parental history of eating pathology showed a greater thalamus and striatum response to milkshake receipt. Conclusions: Overweight/obesity is associated with an elevated reward region response to palatable food cues and food receipt. A risk for eating pathology enhances the reward region response to food cues in those with excess weight.