**1. Introduction**

Obesity is a multifactorial disease involving an interplay between environmental, genetic, biological, and psychological factors [1]. Among them, both homeostatic dysregulation, which results in poor interoceptive awareness and low sensitivity to the physiological hunger and satiety signals [2–4], and emotional dysregulation [5–7] are increasingly being discussed as possible factors involved in non-nutritional eating. Failures in weight management may be partly explained by an incomplete understanding of the psychological obesity risk and maintaining factors [6].

Indeed, while a decrease or suppression of food intake in response to stress and negative mood has been conceived as the natural, typical, distress response because of physiological changes that mimic satiety [8], it is now acknowledged that important individual differences modulate the way people intake food in the same conditions, with as many as 30 to 50% of people who report eating more during stressful periods [9]. Consistently with seminal descriptions of the psychological aspects of hyperphagia and obesity made in the 1950s by Bruch [10], Hamburger [11], and Stunkard [12], and as conceptualized in the Emotionally Driven Eating Model [6,13,14], some individuals appear to be susceptible to unhealthy shifts towards energy-dense and highly palatable (HP) food items when being emotional [15–17]. Both experimental and epidemiological studies on this issue have consistently identified overweight and obese people as being particularly prone to these shifts, and these findings are part of the conceptual framework of the recently proposed Clinical Obesity Maintenance Model [6].

From a neurobiological perspective, it is now established that the regulation of food intake originates from the orchestration of the activity of neural circuits involved in both somatic and affective (or emotional) homeostatic processes. These links have been viewed as the basis for the development of undercontrolled, nonhomeostatic, and addictive-like consumption of high-energy-dense and HP foods [18,19]. While there exists no consensual definition of what should be considered addictive-like eating patterns [20], the concept of food addiction (FA) has been recently identified as a potential underlying mechanism of overeating and unsuccessful attempts to reduce calorie intake [21,22]. Such an eating behavior triggers the neurobiological cascade associated with the brain reward pathways, in a similar way as the association between stress (either intrinsic or extrinsic) and drug addiction [19,23,24].

No standardized definition of emotionally driven eating behaviors exists, but the concept of Emotional eating (EE) is generally defined as the overconsumption of food in response to negative effects rather than in response to feelings of hunger, which places the individual at risk for overweight and obesity [9,25]. Emotional eating has been viewed as a potential precursor of compulsive overeating and addictive-like eating behaviors [26–28] and accumulating evidence suggests that (i) individuals with high levels of negative affectivity are prone to use food for self-medication purposes and to adopt addictive-like eating behaviors [27–30], and (ii) that psychological distress has differential effects on anthropometric indices (BMI, waist circumference and weight gain) as a function of the level of EE or FA (i.e., that emotionally driven and addictive-like eating act as mediators between low mood and high body weight) [28,31,32]. In addition, a diagnosis of FA, as measured by the Yale Food Addiction Scales (YFAS, mYFAS, YFAS2.0, mYFAS2.0), has been found to be positively associated with depression and EE, and FA and EE are prevalent among high BMI populations [33–36]. However, the extent to which these patterns of association are specific to obesity or concerns all weight classes remains largely unexplored.

Different studies have examined emotionally driven and addictive-like eating behaviors in high BMI populations, but the majority of them either included patients seeking bariatric surgery or they did not clearly differentiate obese people from overweight people [33,34]. Of note, besides the prevalence of FA, the question of whether obese and overweight people differ in the type of FA symptoms they endorse has been overlooked. Nonetheless, we suggest that a better understanding of these issues should help to tailor additional therapeutic options.

Accordingly, the aim of the present study was to examine, in a sample from the general population, the extent to which obese people differ in their emotionally driven and addictive-like eating behaviors not only from normal-weight people but also from overweight people. We expected the obese group would present the highest levels of these behaviors and symptoms. Moreover, we expected to observe stronger positive associations between the level of psychological distress and both the EE score and the FA symptoms score and stronger negative associations between the level of psychological distress and the level of sensitivity to the physiological hunger and satiety signals among the obese group than the other two groups.
