Abstract

Background: To explore the theoretical, clinical, and neurobiological underpinnings of obesity as a behavioral addiction and explore the implications for potential inclusion in future DSM (Diagnostic and Statistical Manual of Mental Disorders) revisions. Materials and Methods: A narrative review approach was employed, synthesizing findings from theoretical literature, clinical studies, and neurobiological research examining parallels between obesity and behavioral addiction. Relevant articles were identified through searches of PubMed, PsycINFO, and Google Scholar databases using keywords such as obesity, behavioral addiction, food addiction, compulsive overeating, and reward neurocircuitry. Studies discussing diagnostic frameworks, neurobiological mechanisms, and clinical outcomes were prioritized to inform the review’s objectives. Results: There are striking similarities between patterns of compulsive overeating, and the diagnostic features of substance use disorders. There are several hallmark symptoms associated with addictive disorders that are observable in individuals with obesity. Neurological studies have revealed that the mesolimbic dopamine system, which mediates reward processing, motivation, and reinforcement learning, plays a central role in both substance addiction and maladaptive eating behaviors. An absence of formal diagnostic criteria in current classification systems poses a challenge to effectively classify obesity as the result of addiction and provide targeted intervention. Conclusions: The current review highlights obesity as an outcome of compulsive, addictive eating behaviors with the neurobiological and psychological processes observed in substance use disorders. Conceptualizing certain eating behaviors through the lens of addiction may offer improved clinical utility, particularly for treatment planning and outcome prediction.

1. Introduction

Obesity has emerged as one of the most pressing clinical constructs of the twenty-first century, with complex biological, psychological, and social factors contributing to its persistence and progression. Although traditionally understood through metabolic and lifestyle frameworks, a growing body of research suggests that for a subset of individuals, obesity is driven by patterns of food consumption that resemble features of process addiction. These features include diminished control over intake, persistent desire or unsuccessful efforts to reduce consumption, and continued overeating despite negative consequences [1–3].

Obesity has become one of the most significant public health challenges of the modern era, with global prevalence rates reaching unprecedented levels. Affecting individuals across demographic categories, obesity is commonly approached through a biomedical lens, emphasizing caloric imbalance, sedentary lifestyles, and pharmacological solutions. Yet, this narrow focus overlooks the deeper, more complex origins of excess consumption and body image preoccupations, which are embedded within human cultural evolution, social behaviors, and shifting food environments.

In recent decades, technological advances, the globalization of food production, and the rise of digital media have transformed not only what we eat but also how we perceive food, health, and the human body. Modern societies have cultivated environments where food is not merely a biological necessity but a vehicle for pleasure, identity, and social status. At the same time, the promotion of idealized body images via social networking platforms has intensified selective eating patterns and weight control anxieties, giving rise to restrictive diets and the normalization of anti-obesity therapeutics for both medical and cosmetic purposes.

Neurobiological studies have identified overlapping mechanisms between certain forms of overeating and substance use, particularly in the dysregulation of mesolimbic reward pathways. Functional imaging has demonstrated heightened activation of the striatum in response to food cues and alterations in dopamine signaling that parallel those seen in individuals with substance addiction [4–6]. These findings challenge the rigid division between substance-related and non-substance-related process addictions and support a dimensional model in which overeating may be viewed through the lens of psychological and behavioral addiction.

Currently, gambling disorder remains the only behavioral addiction formally recognized in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; American Psychiatric Association, 2013) [7]. The exclusion of obesity or food addiction from this framework may hinder diagnostic clarity and limit the development of specialized interventions. While we concede that gambling is an unsuitable analogy for eating addiction due to its non-essential characteristics, it is imperative to identify the pervasive long-term effects of excessive eating, necessitating specific classifications to facilitate their recognition within the nosology.

While significant scientific attention has been devoted to treatment paradigms of obesity, a critical and often overlooked question remains inadequately addressed: why are individuals gaining excess weight at such alarming rates in the first place? Beyond simplistic explanations of caloric imbalance, this question demands a multidisciplinary exploration of the social, cultural, and psychological shifts that have transformed human eating behavior and food environments over the last century.

In the last few years, the exponential rise of cultures of diet plans and pharmaceuticals as key solutions to obesity has contributed to a limited view of the disorder that fails to incorporate the behavioral and psychological dimensions of the condition. As a result, individuals may experience temporary weight loss without sustainable, long-term solutions that target the core issues of addiction, emotional eating, or poor self-regulation. Also, these treatment models can inadvertently reinforce the notion that obesity is primarily a metabolic or genetic issue rather than a component of behavioral and psychological manifestations [3].

For healthcare providers and researchers, this situation underscores the critical need for early identification and a more comprehensive approach to obesity management. Addressing obesity as a behavioral addiction, in addition to its medical aspects, allows for a more critical understanding of the condition.

This paper reviews the theoretical, clinical, and neurobiological evidence supporting the reconceptualization of obesity as a behavioral addiction and explores the implications of its potential inclusion in future revisions of the DSM.

2. Materials and methods

This narrative review was conducted to synthesize current theoretical, clinical, and neurobiological literature examining the conceptualization of obesity as a behavioral addiction. Relevant peer-reviewed articles, review papers, and clinical guidelines were identified through searches of the PubMed, PsycINFO, and Google Scholar databases. Search terms included combinations of obesity, behavioral addiction, food addiction, compulsive overeating, reward neurocircuitry, dopamine, and DSM classification. The search was limited to articles published in English between 2000 and 2024 to capture contemporary perspectives and emerging evidence. Additionally, studies in the literature examining the role of pharmacological treatments like GLP-1 receptor agonists in obesity management were reviewed to contextualize the current treatment landscape. Articles discussing limitations in existing classification systems and the implications for clinical practice and DSM revisions were also included.

3. Results

3.1. Conceptual foundations: understanding behavioral addiction

Behavioral addictions refer to patterns of behavior that are characterized by compulsive engagement in rewarding non-substance-related activities, despite adverse consequences, and share key clinical and neurobiological features with substance use disorders. Although the Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM-5) recognizes only gambling disorder within this category, growing evidence supports the inclusion of additional behavioral conditions, such as internet gaming disorder and compulsive sexual behavior, under this conceptual umbrella [7–9].

Core characteristics of behavioral addictions include impaired control over the behavior, increasing priority given to the behavior despite harm, and persistence or escalation over time. These behaviors are frequently preceded by intense craving and are often employed as maladaptive coping mechanisms for emotional distress or negative affective states [10–12]. Chronic engagement in these behaviors may lead to diminished sensitivity to natural reward pathways, increased tolerance to behavioral stimuli, and withdrawal-like symptoms upon cessation, further aligning these syndromes with the neuroadaptive processes observed in substance dependence [13].

Importantly, behavioral addictions overlap with impulse control disorders in their cyclical, reinforcement-driven patterns, rather than being momentary lapses in inhibition. While impulse control disorders such as kleptomania or intermittent explosive disorder are typified by isolated, poorly regulated episodes, behavioral addictions involve sustained preoccupation and functional impairment related to the activity [14–16]. This nuance is central to the evolving classification of compulsive behaviors and underpins the rationale for evaluating certain forms of dysregulated eating as potential behavioral addictions.

The recognition of gambling disorder in DSM-5 as a non-substance-related addiction has opened the door to a broader re-examination of how behavioral patterns, independent of chemical intoxication, can exert addictive effects. This paradigm shift provides a conceptual framework for reconsidering chronic overeating in some individuals not merely as disinhibition or lack of willpower but as a maladaptive behavioral response deeply rooted in the brain’s reward system.

3.2. Clinical overlap between obesity and addictive behaviors

Clinical observations and empirical studies have increasingly documented striking similarities between patterns of compulsive overeating and the diagnostic features of substance use disorders. Individuals with obesity, particularly those who engage in excessive eating or exhibit patterns consistent with persistent inability to control their intake of certain foods despite repeated efforts to do so [1]. This behavioral dysregulation is commonly associated with intense cravings, anticipatory urges, and a narrowing of behavioral repertoire centered around food acquisition and consumption, features that closely mirror the phenomenology of addiction [3].

Several hallmark symptoms associated with addictive disorders are observable in individuals with obesity. These include continued use despite harmful consequences, diminished ability to regulate intake, failed attempts to cut down or abstain, and significant time spent engaging in or recovering from the effects of overeating [17, 18]. Emotional dysregulation also plays a key role; episodes of overeating are often precipitated by stress, anxiety, or dysphoria and may function as maladaptive strategies to manage affective distress, analogous to self-medication patterns in substance use [19, 20]. These behaviors often co-occur with feelings of guilt, shame, and loss of control, leading to further distress and perpetuating a vicious cycle [21, 22].

Tolerance-like phenomena have been reported, wherein individuals require greater quantities of food to achieve the same hedonic satisfaction, particularly with hyperpalatable, high-fat, and high-sugar foods [18]. Similarly, withdrawal-like symptoms, including irritability, restlessness, and mood disturbance, have been documented during attempts to restrict intake or abstain from specific food groups, further reinforcing the addictive nature of certain eating patterns [23].

Notably, these patterns are not universal among individuals with obesity, highlighting the heterogeneity of the condition. Nevertheless, the presence of a process addiction-like phenotype in a subset of individuals with obesity supports the need for a more nuanced clinical taxonomy that distinguishes between purely metabolic forms of obesity and those driven by repetitive behavioral processes. Failure to recognize this distinction may result in inadequate or misaligned treatment strategies that do not address the underlying psychological and neurobiological mechanisms maintaining the maladaptive excessive eating behavior [24].

3.3. Neurobiological evidence supporting addictive models of obesity

Neurobiological research has increasingly demonstrated that the brain circuits implicated in substance use disorders are also activated in individuals who engage in compulsive overeating, particularly in response to highly palatable foods. The mesolimbic dopamine system, which mediates reward processing, motivation, and reinforcement learning, plays a central role in both substance addiction and maladaptive eating behaviors. Functional neuroimaging studies indicate that individuals at risk of obesity exhibit heightened activation in the ventral striatum, amygdala, and orbitofrontal cortex in response to visual and gustatory food cues. In this context, palatable food intake, anticipated intake, and food cues have broad effects, activating additional regions involved in visual attention (inferior parietal lobe, posterior cingulate cortex), gustatory processing (insula, operculum), motor response (precentral gyrus, cerebellum), somatosensory integration (postcentral gyrus), and inhibitory control (inferior frontal gyrus, ventrolateral prefrontal cortex). [4, 5, 25].

This diminished sensitivity to natural rewards may underlie the progressive escalation in intake of highly palatable foods, paralleling the development of tolerance in drug dependence. Moreover, anticipatory dopamine release in response to food-related cues, rather than the actual consumption of food, appears to be a key factor motivating compulsive eating behaviors, reflecting a process of incentive sensitization observed in substance use disorders [26].

Animal models have further substantiated the neuroadaptive changes associated with chronic exposure to highly palatable foods. Rodents given intermittent access to sugar-rich diets exhibit binge-like patterns of consumption, withdrawal-like behaviors upon deprivation, and alterations in dopaminergic and opioid pathways like those seen in drug dependence [27]. These models reinforce the notion that specific combinations of sugar, fat, and salt, commonly found in ultra-processed foods, are capable of hijacking reward pathways in ways that promote compulsive intake [28].

Neurocognitive findings also highlight impaired executive function and reduced prefrontal inhibitory control in individuals with obesity phenotypes. These deficits may contribute to difficulty in regulating impulsive urges and resisting rewarding stimuli, thereby sustaining maladaptive eating behaviors despite awareness of negative health consequences [29]. The convergence of reward hypersensitivity and executive dysfunction mirrors mechanisms identified in other behavioral addictions and lends further support to the conceptualization of a subset of obesity as a neurobehavioral disorder [30].

Taken together, the neurobiological evidence supports the plausibility of an addiction-based model of obesity, particularly in individuals exhibiting compulsive and dysregulated eating behaviors. This framework helps contextualize obesity not only as a metabolic imbalance but also as a disorder of reward processing, with implications for assessment, classification, and treatment.

3.4. Food addiction vs. eating addiction vs. obesity

The terms “food addiction,” “eating addiction,” and “obesity” are often used interchangeably in nonscientific discourse, yet they refer to distinct constructs with important conceptual and clinical implications. While obesity is defined by excessive adiposity as determined by body mass index (BMI), it is a heterogeneous condition with diverse etiologies, including genetic, metabolic, behavioral, and environmental contributors [31]. Not all individuals with obesity demonstrate addictive-like eating behaviors, and conversely, not all individuals exhibiting such behaviors meet criteria for obesity [2].

The concept of food addiction suggests that certain foods, particularly those high in sugar, fat, and salt, possess addictive properties that can directly alter neural reward circuitry, much like psychoactive substances. This model posits that ultra-processed, hyperpalatable foods trigger dopaminergic responses in the brain, reinforcing consumption patterns that become compulsive over time [32, 33]. Proponents of the food addiction model argue that the pharmacological properties of modern food products, engineered for maximal palatability, can drive dependence-like responses, including craving, tolerance, and withdrawal.

In contrast, the eating addiction model emphasizes the behavioral process rather than the properties of the food itself. According to this view, it is not the food that is addictive, but rather the act of eating, often used to modulate affective states or fulfill psychological needs, that becomes compulsive [2]. This distinction aligns with the broader framework of behavioral addictions, in which the compulsive engagement in an activity (e.g., gambling, internet gaming) is central to the disorder, independent of any specific substance. The excessive eating process addiction model highlights the role of emotional dysregulation, learned reinforcement patterns, and impaired inhibitory control as key mechanisms sustaining disordered eating behaviors.

Both perspectives offer valuable insights, yet they diverge in their implications for treatment and nosology. A food addiction model may suggest regulatory policies targeting specific ingredients or food formulations, akin to substance control strategies. In contrast, an eating addiction framework may prioritize behavioral interventions, emotional regulation strategies, and neurocognitive training to address dysregulated consumption. While there is ongoing debate over the most appropriate terminology, emerging consensus suggests that both food- and eating-related addictive behaviors exist along a continuum and may share common mechanisms with, but also differ in meaningful ways from, other psychiatric conditions and, more specifically, serious eating disorder conditions like anorexia nervosa.

Importantly, the presence of addictive-like eating behaviors does not imply that all forms of obesity are rooted in addiction. Obesity may result from a wide range of non-addictive processes, including genetic predispositions, endocrine abnormalities, medication side effects, and sociocultural factors that influence lifestyle and dietary patterns [34, 35]. Recognizing this heterogeneity is crucial to avoid over pathologizing non-hedonic homeostatic eating behavior and to tailor interventions to the specific profiles of affected individuals. It is also critical to note that, while these two constructs are phenomenologically different, they are likely to coexist, and the model should not be inclined to focus on mutually exclusive dualism but complex interplay to formulate and develop treatment models.

3.5. Assessment and diagnostic challenges

The clinical assessment of overeating behaviors presents unique challenges, particularly given the absence of formal diagnostic criteria in current classification systems. Unlike substance use disorders, where clear criteria are delineated in the DSM-5, there is no consensus regarding the threshold for disordered eating, nor is there agreement on whether these constructs represent distinct disorders or phenotypic expressions within broader categories such as obesity [7, 36].

One of the most widely used instruments to assess food addiction is the Yale Food Addiction Scale (YFAS), which operationalizes addiction-like eating based on DSM-IV criteria for substance dependence. The YFAS has demonstrated reliability and predictive validity, identifying a subset of individuals with obesity or disordered eating who exhibit symptoms such as loss of control, tolerance, withdrawal, and continued use despite adverse consequences [1]. However, criticisms of the YFAS highlight potential limitations, including its reliance on self-report, the overlap with other eating disorder diagnoses, and the ambiguity in interpreting behaviors like “tolerance” in the context of food intake [17].

Differentiating food addiction from established eating disorders, particularly binge eating disorder (BED), is another source of diagnostic complexity. Although there is significant symptom overlap, including episodes of excessive intake and loss of control, food addiction is conceptualized as a chronic, trait-like vulnerability that may or may not co-occur with discrete binge episodes [25].

Food addiction and binge eating disorder (BED) share overlapping clinical features, including impaired control over intake, persistent overconsumption despite adverse consequences, and compulsive eating patterns reminiscent of substance dependence [37–39]. Animal models provide additional support for this parallel; for instance, Johnson and Kenny demonstrated that rats granted access to highly palatable, sugar-rich diets continued to consume such foods despite receiving electric shocks [40]. These animals not only developed obesity but also exhibited downregulated dopamine D2 receptor expression in the striatum, a neuroadaptation commonly associated with drug addiction [40].

BED is diagnosed when individuals engage in recurrent binge episodes (i.e., at least once weekly for three months), often triggered by psychological distress and followed by feelings of guilt or shame [8]. In contrast, food addiction, although not formally recognized in the DSM-5, is typically assessed using the Yale Food Addiction Scale (YFAS) and is characterized by addiction-like symptoms such as craving, tolerance, withdrawal, and significant impairment in functioning [41, 42].

Despite their similarities, these disorders differ in key domains. BED is generally episodic and emotionally driven, whereas food addiction tends to reflect a more chronic and compulsive pattern of consumption, frequently involving specific hyperpalatable foods [32]. Individuals with BED often maintain insight into their behavior and may attempt to moderate eating in public or express concerns about weight and caloric intake [43]. Conversely, those with food addiction may display psychological defenses such as denial or minimization and continue maladaptive eating patterns across various social settings [44].

Additionally, physiological markers of addiction such as tolerance and withdrawal are commonly observed in cases of food addiction but are typically absent in BED [3]. These distinctions suggest differing underlying mechanisms, despite shared behavioral outcomes.

Also, individuals with BED do not necessarily exhibit addictive-like neural or behavioral patterns, and not all individuals who endorse food addiction symptoms meet criteria for BED, suggesting these conditions may represent partially overlapping but distinct constructs [45].

The lack of formal diagnostic recognition in DSM or ICD systems also creates challenges for clinical practice and research standardization [46]. Without a clear nosological status, individuals with excessive eating behavioral addiction phenotypes may be misclassified, underdiagnosed, or inappropriately treated using models designed for other disorders. Moreover, the sociocultural stigma associated with both obesity and addiction can influence self-perception and clinician attitudes, potentially affecting the validity of assessments and the therapeutic alliance.

Incorporating neurobiological, behavioral, and psychosocial data into diagnostic criteria may enhance the specificity and utility of future classifications. As research continues to clarify the distinctiveness and clinical utility of the food addiction construct, the field must remain cautious in avoiding over pathologization while still acknowledging the profound impairment and distress that these behaviors can cause in affected individuals.

3.6. Implications for classification in Diagnostic and Statistical Manual of Mental Disorders

The inclusion of behavioral addictions in the DSM-5, beginning with gambling disorder and subsequently internet gaming disorder (as a condition warranting further study), has opened the door for the broader consideration of non-substance-related addictive behaviors within psychiatric nosology [7]. Given the accumulating evidence of neurobiological, behavioral, and clinical parallels between compulsive eating and substance use disorders, the argument for classifying a subtype of obesity or disordered eating as a behavioral process addiction within the DSM framework may be needed.

The primary rationale for such inclusion rests on empirical observations that addictive-like eating behaviors fulfill many of the established diagnostic criteria for substance use disorders, including craving, loss of control, continued use despite harm, tolerance, and withdrawal-like symptoms [1]. Moreover, the engagement of similar neurocircuitry, particularly mesolimbic dopaminergic pathways and the prefrontal cortex, supports the validity of a shared neurobiological underpinning [3]. These findings suggest that conceptualizing certain eating behaviors through the lens of addiction may offer improved clinical utility, particularly for treatment planning and outcome prediction.

Nevertheless, challenges to DSM inclusion remain. There is apprehension about medicalizing normative or culturally influenced eating behaviors, particularly in the absence of clear thresholds for pathology [2]. Critics also caution against overextending the addiction model to encompass a wide range of dysregulated behaviors, potentially diluting the specificity and rigor of psychiatric classification [47].

Despite these concerns, incorporating a formal diagnostic entity such as “food addiction disorder” into the DSM could catalyze the development of targeted assessments, stimulate research into specific treatment modalities, and validate the experiences of individuals whose excessive eating is poorly explained by current diagnostic categories. Drawing on the precedent set by other behavioral addictions, such a classification could initially be introduced as a condition for further study, pending the accumulation of more robust longitudinal, neurobiological, and epidemiological data.

Ultimately, the consideration of addictive models of eating within DSM classification must balance scientific validity, clinical utility, and the potential impact on stigma and public health policy. As evidence continues to mount, psychiatric nosology must remain adaptable to the evolving understanding of how brain–behavior relationships underpin complex conditions such as obesity and disordered eating. Table 1 contrasts medical and behavioral approaches in a structured manner, offering insight into why both are important for a comprehensive treatment plan and why behavioral addiction should be incorporated into the DSM for more effective treatment.

Table 1

A rationale for adding behavioral addictions to the DSM: implications for clinical recognition and treatment.

Aspect	Medical approach	Behavioral approach
Focus	Treatment of obesity as a primarily medical condition, emphasizing weight reduction through pharmacological or surgical means.	Focus on the psychological and behavioral factors contributing to obesity, such as emotional eating, food addiction, and poor self-regulation.
Treatment methods	Dietary modifications, medications (e.g., Ozempic, GLP-1 agonists), bariatric surgery, and weight loss interventions.	Cognitive Behavioral Therapy (CBT), mindfulness techniques, motivational interviewing, and support groups.
Primary goal	Reduce weight and improve metabolic health (e.g., blood pressure, cholesterol).	Change unhealthy eating behaviors, improve emotional regulation, and address underlying psychological factors.
Short-term effectiveness	Immediate reduction in weight and improvements in associated metabolic conditions.	Gradual improvement in eating habits, long-term weight management, and emotional coping mechanisms.
Long-term effectiveness	Weight loss may be temporary, especially if behavioral factors remain unaddressed.	Focus on sustainable changes in behavior and emotional health, leading to more lasting outcomes.
Limitations	Does not address the root causes of obesity, and may result in regaining weight if psychological factors are not treated.	May require more time and sustained effort to see significant weight reduction, and is often seen as more difficult for individuals to engage with initially.
Pharmaceutical influence	Strong influence of pharmaceutical companies promoting medications as primary solutions.	Less influence from pharmaceutical companies but relies on evidence-based therapies for psychological and behavioral changes.
Role of DSM	Obesity is currently not classified as a behavioral addiction in the DSM, though some view it as an addiction.	Recognizes obesity as potentially involving addictive behaviors that should be included in the DSM for more comprehensive treatment approaches.
Critical view	Focuses on symptom management rather than addressing the underlying psychological issues, possibly leading to cycles of weight loss and regain.	Focuses on understanding and addressing the core behavioral and emotional issues contributing to obesity, offering a more holistic, long-term solution.
Recommended integration	Can be integrated with behavioral approaches for better holistic management.	Should be recognized alongside medical treatments to ensure the underlying behavioral factors are also addressed.

4. Discussion

An association between food addiction, obesity and functional impairments is evident. These patterns mirror trajectories seen in other behavioral addictions, suggesting that eating behavior moves beyond homeostatic survival needs and moves to a hedonic reward-driven pattern. The conceptualization of certain forms of obesity as behavioral addictions has profound implications for treatment strategies. Traditional approaches to obesity have predominantly focused on dietary management, physical activity, and pharmacological interventions aimed at modifying metabolic processes. However, the behavioral model may necessitate more integrated psychological modalities.

Cognitive Behavioral Therapy (CBT) has been widely used to address the psychological and behavioral components of obesity, particularly in individuals exhibiting binge eating behaviors. CBT techniques, such as cognitive restructuring, self-monitoring, and stimulus control, aim to reduce maladaptive eating patterns and enhance self-regulation. In the context of food addiction, CBT may need to be adapted to incorporate strategies that specifically address compulsive food seeking, craving, and emotional dysregulation [48, 49]. For instance, therapies focusing on emotional regulation and impulse control, like those used in the treatment of substance use disorders, may be effective in modulating the psychological triggers that drive excessive eating [8].

Recent advances in the pharmacological management of obesity and disordered eating have prompted renewed interest in addiction-informed treatment frameworks. While currently approved anti-obesity agents including orlistat, liraglutide, and phentermine primarily exert their effects through peripheral metabolic pathways (e.g., inhibition of fat absorption, appetite suppression via incretin mimetics), they fail to directly target the central neurobiological mechanisms implicated in compulsive food consumption and reward dysregulation [50]. This limitation has spurred the exploration of centrally acting agents aimed at modulating mesolimbic dopamine pathways and other neurochemical systems involved in addictive behavior.

Emerging evidence suggests that selective serotonin reuptake inhibitors (SSRIs) and opioid antagonists, such as naltrexone, may attenuate hedonic drive and reduce the frequency of binge eating episodes through their effects on serotonergic and endogenous opioid signaling [51]. More recently, glucagon-like peptide-1 (GLP-1) receptor agonists, particularly semaglutide, have demonstrated efficacy not only in glycemic regulation and appetite suppression but also in modulating neural activity within the brain’s reward circuitry, including regions such as the nucleus accumbens and ventral tegmental area. This dual-action profile underscores their potential utility in addressing both homeostatic and hedonic aspects of disordered eating [52].

Tirzepatide, a novel dual GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) receptor agonist, has further expanded therapeutic possibilities. Preclinical and early clinical data indicate that tirzepatide may exert synergistic effects on energy intake, satiety signaling, and reward-related neural activation. Importantly, it is being actively investigated for applications beyond obesity, including substance use disorders, due to its favorable safety profile and broad modulatory effects on central appetite pathways [53].

Nonetheless, the durability of pharmacotherapy remains challenged by compensatory physiological adaptations upon treatment discontinuation. Hormonal responses such as elevated ghrelin and suppressed leptin levels promote increased hunger and diminished satiety, contributing to weight regain and possible relapse into compulsive eating patterns [54]. These adaptive responses emphasize the necessity for long-term, integrated treatment approaches that combine pharmacological, behavioral, and possibly neuromodulatory strategies to ensure sustained remission of addiction-like eating behaviors.

Additionally, medications targeting dopamine or other neurotransmitter systems implicated in addiction, such as modafinil or bupropion, may be useful in treating individuals with food addiction symptoms, although more research is needed to establish their efficacy [55]. Neurobiological interventions are an emerging area of interest, particularly in the form of neuromodulation techniques such as transcranial magnetic stimulation (TMS) or deep brain stimulation (DBS). These approaches have shown promise in treating addiction by modulating neural circuits involved in reward processing and impulse control [56]. Applied to food addiction, these techniques could potentially reduce craving and compulsive eating behaviors by modulating activity in the mesolimbic dopamine system or prefrontal cortex, regions implicated in both food addiction and substance use disorders.

For individuals with a food addiction phenotype, treatment may involve a combination of behavioral therapies, pharmacological interventions, and nutritional counseling [57].

The inclusion of food addiction in diagnostic frameworks such as the DSM will undoubtedly spur further research into the most effective treatment strategies. Longitudinal studies exploring the neurobiological, psychological, and behavioral trajectories of individuals with food addiction symptoms will be critical in refining diagnostic criteria and treatment modalities. Additionally, more research is needed to explore the role of genetic and environmental factors in the development of food addiction, as this information could inform personalized treatment approaches and preventative strategies [58].

Ultimately, the treatment of obesity and disordered eating from an addiction-based perspective holds promise for improving outcomes, particularly for individuals whose symptoms are driven by compulsive and dysregulated behaviors. However, future research must continue to refine the constructs of food addiction, clarify their neurobiological underpinnings, and validate the effectiveness of targeted interventions before these concepts are fully integrated into clinical practice.

5. Conclusions

The emerging conceptualization of obesity as a behavioral addiction holds significant potential for advancing both our understanding and treatment of this complex condition. As evidence accumulates supporting the addictive-like characteristics of certain eating behaviors, it becomes increasingly clear that obesity is not solely a result of poor dietary choices or lifestyle factors.

However, the integration of food addiction into formal diagnostic frameworks such as the DSM remains a contentious issue. While the neurobiological, behavioral, and clinical parallels between addiction and disordered eating behaviors are compelling, there is still insufficient consensus on whether these behaviors represent a distinct disorder or fall within the spectrum of etiological factors for obesity. Further research is essential to clarify the underlying mechanisms and delineate the boundaries of these constructs, which will ultimately inform the diagnostic criteria and treatment protocols.

The potential for incorporating food addiction into clinical practice is vast. If recognized and classified appropriately, it could lead to more tailored treatment approaches, including pharmacological interventions targeting reward systems, behavioral therapies addressing compulsive eating, and care models that integrate psychological, medical, and nutritional support.

In conclusion, the integration of food addiction into psychiatric classification systems holds promise for improving the clinical management of obesity. As the field progresses, ongoing research into the neurobiological, psychological, and environmental contributors to these evolving constructs will enhance our ability to provide more effective, individualized care for individuals suffering from this multifaceted condition.

Funding

This research received no external funding.

Author contributions

Conceptualization, M.G. and N.G.; methodology, N.G. and P.K.; formal analysis, N.G., M.G., and P.K.; data curation, N.G. and P.K.; writing—original draft preparation, M.G., N.G., and P.K.; writing—review and editing, M.G. and P.K.; supervision, M.G. and N.G. All authors have read and agreed to the published version of the manuscript.

Conflict of interest

The authors declare that they have no competing interests.

Data availability statement

All data supporting the findings of this publication are available within this article.

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References

1

Gearhardt AN, Corbin WR, Brownell KD. Food addiction: an examination of the diagnostic criteria for dependence. J Addict Med. 2009;3(1):1–7. doi: 10.1097/ADM.0b013e318193c993

2

Hebebrand J, Albayrak Ö, Adan R, Antel J, Dieguez C, de Jong J, et al. “Eating addiction”, rather than “food addiction”, better captures addictive-like eating behavior. Neurosci Biobehav Rev. 2014;47:295–306. doi: 10.1016/j.neubiorev.2014.08.016

4

Ng M, Gakidou E, Lo J, Abate YH, Abbafati C, Abbas N, et al. Global, regional, and national prevalence of adult overweight and obesity, 1990–2021, with forecasts to 2050: a forecasting study for the global burden of disease study 2021. Lancet. 2025;405(10481):813–38. doi: 10.1016/S0140-6736(25)00355-1

5

Tanwar N, Kumar S, Choudhary S. Impact of technology on daily food habits and their effects on health. In: Optimized predictive models in healthcare using machine learning. Hoboken (NJ): John Wiley & Sons, Ltd.; 2024. p. 1–20. doi: 10.1002/9781394175376.ch1

6

García-Castro J, Cancela A, Cárdaba MAM. Neural cue-reactivity in pathological gambling as evidence for behavioral addiction: a systematic review. Curr Psychol. 2023;42(32):28026–37. doi: 10.1007/s12144-022-03915-0

7

Batat W, Peter PC, Moscato EM, Castro IA, Chan S, Chugani S, et al. The experiential pleasure of food: a savoring journey to food well-being. J Bus Res. 2019;100:392–9. doi: 10.1016/j.jbusres.2018.12.024

8

American Psychiatric Pub. Diagnostic and statistical manual of mental disorders (DSM-5®). Washington (DC): American Psychiatric Pub; 2013.

9

Sixto-Costoya A, Castelló-Cogollos L, Aleixandre-Benavent R, Valderrama-Zurián JC. Global scientific production regarding behavioral addictions: an analysis of the literature from 1995 to 2019. Addict Behav Rep. 2021;14:100371. doi: 10.1016/j.abrep.2021.100371

10

Lee NM, Carter A, Owen N, Hall WD. The neurobiology of overeating. EMBO Rep. 2012;13(9):785–90. doi: 10.1038/embor.2012.115

11

Rand K, Vallis M, Aston M, Price S, Piccinini-Vallis H, Rehman L, et al. “It is not the diet; it is the mental part we need help with.” A multilevel analysis of psychological, emotional, and social well-being in obesity. Int J Qual Stud Health Well-Being. 2017;12(1):1306421. doi: 10.1080/17482631.2017.1306421

13

Hunt A, Merola GP, Carpenter T, Jaeggi AV. Evolutionary perspectives on substance and behavioural addictions: distinct and shared pathways to understanding, prediction and prevention. Neurosci Biobehav Rev. 2024;159:105603. doi: 10.1016/j.neubiorev.2024.105603

14

Brand M, Wegmann E, Stark R, Müller A, Wölfling K, Robbins TW, et al. The Interaction of Person-Affect-Cognition-Execution (I-PACE) model for addictive behaviors: update, generalization to addictive behaviors beyond internet-use disorders, and specification of the process character of addictive behaviors. Neurosci Biobehav Rev. 2019;104:1–10. doi: 10.1016/j.neubiorev.2019.06.032

15

Grant JE, Potenza MN, Weinstein A, Gorelick DA. Introduction to behavioral addictions. Am J Drug Alcohol Abuse. 2010;36(5):233–41. doi: 10.3109/00952990.2010.491884

16

Chatzittofis A, Kim HS. Editorial: behavioral addictions: emerging science. Front Psychiatry. 2023;13:1127444. doi: 10.3389/fpsyt.2022.1127444

17

Koob GF, Volkow ND. Neurobiology of addiction: a neurocircuitry analysis. Lancet Psychiatry. 2016;3(8):760–73. doi: 10.1016/S2215-0366(16)00104-8

18

Ferrer-Pérez C, Montagud-Romero S, Blanco-Gandía MC. Neurobiological theories of addiction: a comprehensive review. Psychoactives. 2024;3(1):35–47. doi: 10.3390/psychoactives3010003

19

Volkow ND, Wang GJ, Baler RD. Reward, dopamine and the control of food intake: implications for obesity. Trends Cogn Sci. 2011;15(1):37–46. doi: 10.1016/j.tics.2010.11.001

20

Hanßen R, Schiweck C, Aichholzer M, Reif A, Edwin Thanarajah S. Food reward and its aberrations in obesity. Curr Opin Behav Sci. 2022;48:101224. doi: 10.1016/j.cobeha.2022.101224

21

Snoek A, McGeer V, Brandenburg D, Kennett J. Managing shame and guilt in addiction: a pathway to recovery. Addict Behav. 2021;120:106954. doi: 10.1016/j.addbeh.2021.106954

22

Batchelder AW, Glynn TR, Moskowitz JT, Neilands TB, Dilworth S, Rodriguez SL, et al. The shame spiral of addiction: negative self-conscious emotion and substance use. PLoS ONE. 2022;17(3):e0265480. doi: 10.1371/journal.pone.0265480

23

Gearhardt AN, Di Feliceantonio AG. Highly processed foods can be considered addictive substances based on established scientific criteria. Addiction. 2023;118(4):589–598. doi: 10.1111/add.16065

24

Schultes B, Ernst B, Hallschmid M, Bueter M, Meyhöfer SM. The ‘Behavioral Balance Model’: a new perspective on the aetiology and therapy of obesity. Diabetes Obes Metabolism. 2023;25(12):3444–52. doi: 10.1111/dom.15271

25

Stice E, Spoor S, Bohon C, Small DM. Relation between obesity and blunted striatal response to food is moderated by TaqIA A1 allele. Science. 2008;322(5900):449–52. doi: 10.1126/science.1161550

26

Davis C, Curtis C, Levitan RD, Carter JC, Kaplan AS, Kennedy JL. Evidence that ‘food addiction’ is a valid phenotype of obesity. Appetite. 2011;57(3):711–7. doi: 10.1016/j.appet.2011.08.017

27

Anderson LM, Hall LMJ, Crosby RD, Crow SJ, Berg KC, Durkin NE, et al. “Feeling fat,” disgust, guilt, and shame: preliminary evaluation of a mediation model of binge-eating in adults with higher-weight bodies. Body Image. 2022;42:32–42. doi: 10.1016/j.bodyim.2022.05.008

28

Morys F, Kanyamibwa A, Fängström D, Tweedale M, Pastor-Bernier A, Azizi H, et al. Ultra-processed food consumption affects structural integrity of feeding-related brain regions independent of and via adiposity. Npj Metab Health Dis. 2025;3:13. doi: 10.1038/s44324-025-00056-3

29

Krug I, Dang AB, Lu E, Ooi WL, Portingale J, Miles S. A narrative review on the neurocognitive profiles in eating disorders and higher weight individuals: insights for targeted interventions. Nutrients. 2024;16(24):4418. doi: 10.3390/nu16244418

30

Sutton CA, L’Insalata AM, Fazzino TL. Reward sensitivity, eating behavior, and obesity-related outcomes: a systematic review. Physiol Behav. 2022;252:113843. doi: 10.1016/j.physbeh.2022.113843

31

Mayoral LPC, Andrade GM, Mayoral EPC, Huerta TH, Canseco SP, Rodal Canales FJ, et al. Obesity subtypes, related biomarkers & heterogeneity. Indian J Med Res. 2020;151(1):11–21. doi: 10.4103/ijmr.IJMR_1768_17

32

Schulte EM, Avena NM, Gearhardt AN. Which foods may be addictive? Th