This study emerged from a fundamental puzzle in eating-behaviour research: why do some individuals with obesity exhibit patterns of compulsive food consumption and psychological symptoms that resemble addiction, while others with similar body mass index (BMI) do not? Although the concept of food addiction has gained interest in recent decades, it remains controversial and poorly understood, especially at a biological level. Traditional explanations often focus on calorie balance, environmental exposure to processed foods, or psychosocial stressors alone. With this study we wanted to integrate genetic mechanisms into this broader picture to see whether variation in genes known to regulate appetite and reward might help explain individual differences in addictive-like eating behaviour.
The investigation focuses on the melanocortin-4 receptor (MC4R) gene, which plays a key role in the brain’s regulation of satiety, reward, and energy balance. Prior studies have linked MC4R variants to obesity and eating behaviours, but direct genetic associations with clinically defined food addiction had not yet been rigorously tested among people with obesity. By genotyping multiple MC4R polymorphisms (including rs17782313) in a clinical sample of people seeking weight-loss treatment and comparing those with versus without food addiction based on validated diagnostic scales, our group aimed to bridge molecular variation with behavioural phenotype.
The main finding was relevant: one MC4R variant (rs17782313) showed a robust association with food addiction. Specifically, carriers of the C allele were not only more likely than non-carriers to meet criteria for food addiction, and, noteworthy, they also had higher levels of anxiety and depressive symptoms, dimensions that are often intertwined with compulsive eating.This finding suggests that genetic variation in a key appetite regulation pathway contributes not only to patterns of loss of control over eating but also to associated affective symptoms.
Scientifically, these results underscore that eating behaviours and obesity are not reducible to simple external factors or conscious decision making alone. Instead, individual biological predispositions interact with psychological and environmental influences to shape how people respond to food rewards and regulate intake. The results encourage moving beyond a purely behavioural or environmental framing of obesity, positioning genetic insights as a tool for more nuanced risk stratification and potentially tailored interventions.
From a clinical point of view, the study stresses the importance of recognizing heterogeneity within obesity as some patients may struggle with patterns resembling addiction because of inherent differences in reward-related circuitry, not just lifestyle or willpower. Understanding these peculiarities can help refine assessment, reduce stigma, and design supportive interventions that account for underlying biological vulnerabilities.
In essence, the paper invites the clinicians and researchers to rethink food addiction from a metaphor derived from substance use to a genetic-informed behavioural phenotype that, if validated in future studies, could link molecular neuroscience with real-world therapeutic strategies.