Intermittent fasting (IF) has emerged as a potential strategy to address the impact of the current obesogenic environment, where the abundance of ultra-processed and highly palatable foods deeply activates the mesocorticolimbic circuit, enhancing their rewarding properties. IF decreases cravings and preferences for unhealthy foods. Mechanistically, IF modulates homeostatic responses in the hypothalamus and also dopaminergic activity within the reward system. Additionally, IF is linked to reductions in neuroinflammation and increases in neurotrophic factors such as brain-derived neurotrophic factor (BDNF), which support brain plasticity during reward for palatable foods. Current evidence in humans has started to decode the role of IF protocols and assess their long-term impact on homeostatic and food reward related to metabolic health. This review article will contribute to defines how IF modulates molecular and cellular plasticity to influence eating behavior by reducing the reward value and setting homeostatic responses for food.
Pérez‐Kast et al. (2025) studied this question.