To examine whether ultraprocessed food (UPF) intake is associated with striatal responses to food cues and subsequent changes in adiposity among children of healthy weight.
Approach:
Participants and measures: Researchers analyzed 46 children aged 7–10 years in the longitudinal BrainChild cohort. Baseline assessments included two 24-hour dietary recalls, food-cue functional MRI, and anthropometric measurements; adiposity was reassessed about one year later.
Analysis: Models examined UPF intake, striatal responses, and changes in BMI, body fat percentage (BFP), and waist circumference, adjusting for age, sex, baseline BMI, caloric intake, and prenatal gestational-diabetes exposure.
Key Findings:
UPFs provided an average of 67.7% of participants’ daily calories.
Higher UPF intake was associated with greater dorsal striatal responses to food cues; no significant association was found in the ventral striatum.
Greater baseline dorsal striatal responses were associated with larger one-year increases in BMI and BFP, but not waist circumference.
Higher UPF intake was associated with greater waist circumference increases. Its associations with BMI and BFP increases were positive but did not clearly reach statistical significance.
Accounting for dorsal striatal responses attenuated estimated UPF associations with BMI and BFP gains by 31% and 44%, respectively; no formal mediation analysis was conducted.
In post hoc analyses, added sugar was not significantly associated with striatal responses, but adjusting for it made the UPF–dorsal striatal association no longer statistically significant.
Interpretation:
The authors described the findings as suggesting that greater UPF consumption may be associated with motivational and habit-based neural processes, rather than hedonic valuation alone. The observational results do not establish causal direction.
Limitations:
The small sample limited statistical power and raised concerns about reproducibility.
Dietary intake was based on participant and parent recall, and brain responses were measured at only one time point.
The food-cue task did not account for individual food preferences or assess behavioral reward sensitivity; food insecurity was not evaluated.
The healthy-weight-only cohort limits generalizability to children with overweight or obesity.
The observational design cannot determine whether UPF intake changes brain responses or whether pre-existing neural differences influence food intake.
Conclusion:
The authors called for larger longitudinal studies with repeated neuroimaging to clarify the direction and persistence of these associations. The study does not establish whether changing UPF intake would prevent adiposity gain.
