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Reward-related eating behavior, also known as hedonic eating, refers to the consumption of food driven by the brain's reward system rather than metabolic energy needs. This process is primarily mediated by the mesocorticolimbic dopamine pathway, which regulates the motivation or 'wanting' of food, and the endogenous opioid system, which influences the 'liking' or palatability of energy-dense foods [3, 6]. In modern environments where highly palatable, calorie-rich foods are abundant, reward-related signals can override homeostatic satiety cues, leading to overconsumption and weight gain [1, 4]. This behavior is a central feature in the pathophysiology of obesity, binge eating disorder, and food addiction [7, 8]. Pharmacological interventions targeting this behavior typically involve modulating neurotransmitter systems—such as dopamine, opioids, and GLP-1—to reduce food cravings, decrease the reinforcing properties of food, and improve inhibitory control over eating impulses [1, 11].
Pharmacological modulation of reward-related eating involves antagonizing opioid receptors to reduce food palatability, increasing synaptic dopamine/norepinephrine to reduce cravings and improve inhibitory control, or activating GLP-1 receptors to enhance satiety and dampen mesolimbic reward signaling [1, 3, 16].
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