Triglycerides and Food Reward Signaling in Binge Eating Disorder

Abstract

Emerging research increasingly suggests that triglycerides influence dopamine pathways, impacting appetite regulation and reinforcing binge-eating behaviors. To investigate this, we recruited 61 female participants categorized into three groups: patients with BED, subsyndromal BED, and a control group. Each participant completed two in-lab sessions, including diagnostic interviews, behavioral assessments, blood draws, and reward-related tasks while undergoing MRI scans. During the study, participants performed a FCR task, measuring BOLD response amplitudes and functional connectivity during a food bidding task. Neural activity was then analyzed in relation to triglyceride levels obtained from blood samples. Our hypothesis was that elevated plasma triglyceride levels would be associated with a reduced neural response to palatable food cues. Through our findings, we were able to confirm this hypothesis, showing that while individuals with BED exhibit heightened activation in reward-related brain regions, elevated triglyceride levels correlate with a blunted response in key reward processing areas. Subsyndromal BED participants displayed intermediate activation, suggesting a continuum of reward sensitivity in binge eating behaviors. Notably, higher fasting triglyceride levels were linked to reduced activation in brain regions involved in reward processing, interoception, and memory. Significant negative correlations between triglyceride levels and activation in the insula and hippocampus suggest that metabolic dysregulation may dampen neural responsiveness to food-related stimuli. Additionally, greater post-meal triglyceride fluctuations were associated with attenuated activation in regions critical for dopamine signaling and reward regulation. These findings suggest that chronic overconsumption and metabolic alterations may lead to a gradual desensitization of the brain’s reward system. Overall, our findings highlight the critical role of metabolic factors in shaping neural responses to food. Understanding these mechanisms could enable targeted interventions aimed at restoring reward sensitivity and improving appetite regulation in individuals with BED. Future research should explore how metabolic modulation may serve as a potential therapeutic strategy for disordered eating behaviors.