Triangulating Causality Between Childhood Obesity and Neurobehavior: Twin and Longitudinal Evidence

Abstract

Childhood obesity is a serious health concern that is not yet fully understood. Previous research has linked obesity with neurobehavioral factors such as behavior, cognition, and brain morphology. The causal directions of these relationships remain mostly untested. Here, we filled this gap by using the Adolescent Brain Cognitive Development study cohort comprising 11,875 children aged nine to ten. Cross-sectionally, body mass percentile correlated with measures of impulsivity, motivation, psychopathology, eating behavior, and cognitive tests (executive functioning, language, memory, perception, working memory). Obesity was associated with reduced cortical thickness in areas of the frontal and temporal lobe but with increased thickness in parietal and occipital brain areas. Similar although weaker patterns emerged for cortical surface area and volume. Effects for each neurobehavioral factor (personality/psychopathology, eating behavior, cognition, cortical thickness, cortical surface area, and cortical volume) were then aggregated for causal analyses. Direction of Causation twin modeling was used to test the direction of each relationship. Findings were validated by longitudinal analyses. Twin modeling suggested causal effects of childhood obesity on eating behavior (β=.26), cognition (β=.05), cortical thickness (β=.15), and cortical surface area (β=.07). Personality/psychopathology (β=.09) and eating behavior (β=.16) appeared to causally influence childhood obesity. Longitudinal evidence broadly supported these findings. Results regarding cortical volume were inconsistent. In summary, childhood obesity had considerable causal effects on brain functioning and morphology, supporting the brain inflammation theory. The present study highlights the importance of physical health for brain development during childhood and may inform interventions aimed at preventing or reducing pediatric obesity.