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Food as Addiction: Understanding Obesity Through a New Neurobiological Lens

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dr. Karunia Valeriani Japar

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Introduction

Obesity has traditionally been understood as the result of a complex interplay between genetic, behavioural, and environmental influences, with excessive caloric intake and sedentary lifestyles serving as key contributors. However, emerging research now conceptualizes a significant subset of obesity as potentially rooted in addictive processes linked to food consumption. The theory of “food addiction” proposes that certain highly palatable, often high-glycemic-index foods possess properties capable of hijacking neurobiological pathways involved in reward, impulse control, and motivation, paralleling those implicated in substance abuse disorders. This paradigm shift expands the definition of addiction beyond illicit drugs and alcohol, encompassing compulsive eating behaviours that persist despite known negative consequences.

Food addiction is characterized by symptom clusters, such as intense cravings, repeated loss of control over intake, persistent efforts to cut down, and withdrawal-like symptoms when attempting to reduce consumption, that closely mirror those observed in substance use disorders. These addictive responses are especially pronounced with foods high in refined carbohydrates and sugars, which induce rapid fluctuations in blood glucose and insulin levels, reinforcing maladaptive eating patterns. Neuroimaging studies further demonstrate that the consumption and anticipation of such foods active reward-related brain regions including striatum and orbitofrontal cortex, supporting the neurobiological overlap between food and substance addiction.

Growing evidence suggests that recognition of “food addiction” as a distinct etiological factor may offer novel insights into both the pathophysiology and clinical management of obesity, requiring integrated strategies that address both biological vulnerabilities and behavioural interventions.

Evolution of Addiction: from Substances to Food

Historical Perspective: Addiction and Substance Use Disorders

The conceptualization of addiction has deep historical roots, with early research and societal concern predominantly focused on the misuse psychoactive substances such as morphine, cocaine and opium. Pioneering studies in the late 19th and early 20th centuries sought to characterize addiction as medical condition, identifying hallmark behaviours such as compulsive drug seeking, prioritization of substance use over other life needs, and the phenomenon of withdrawal symptoms upon cessation. Over subsequent decades, as patterns of substance use evolved, so did the approaches to addiction, from punitive models centered on law enforcement to recognition of substance use disorders as chronic medical diseases with complex biological, psychological and social underpinnings [1.2.3].

Expansion of Addiction Theory to Include Compulsive Eating Behaviours

Recent decades have witnessed a significant expansion of addiction frameworks to include compulsive behaviours beyond classical drug abuse, notably in the area of highly palatable food consumption. Research in neural circuitry has demonstrated that behaviours such as pathological overeating engage reward pathways paralleling those activated by drugs of abuse, implicating systems within the basal ganglia, extended amygdala, and prefrontal cortex in both conditions. These neurobiological overlaps, together with behavioural similarities such as conditioned reinforcement, maladaptive habit formation, and affective “withdrawal”, have led to the proposal that certain eating behaviours, particularly in response to hyper-palatable, high-sugar, or high-GI foods, constitute a form of behavioural addiction [4,5,6].

Key Diagnostic Criteria for Food Addiction

The diagnostic criteria for food addiction have been largely adapted from those used for substance use disorders, especially as formally outlined in the DSM-5. Key features include impaired control over consumption, persistent desire or repeated unsuccessful efforts to cut down, continued use despite adverse consequences, intense craving or preoccupation, and withdrawal-like symptoms such as irritability or negative mood when attempting to reduce intake. Instruments such as the Yale Food Addiction scale (YFAS 2.0) operationalize these criteria, requiring the fulfilment of at least two of the eleven substance related and addictive disorder criteria alongside significant impairment or distress for a diagnosis. This evolving diagnostic framework underlines the increasing recognition of food addiction as a relevant construct with both clinical and public health implications [7,8,9,10].

Neurobiological Pathways Shared by Food and Drug Addiction

The Mesolimbic Dopamine System and Reward Processing

The mesolimbic dopamine system, comprising dopaminergic projections from the ventral tegmental area (VTA) to the nucleus accumbens (NAc) and interconnected limbic and cortical structures, serves as the primary neural circuit mediating motivation, reinforcement, and reward-related behaviour. Both food consumption and drug administration activate this reward pathway, resulting in phasic dopamine release in the NAc that correlates with the subjective experience of pleasure and reinforcement. Consumption of highly palatable foods, particularly those rich in sugar, fat, and refined carbohydrates, triggers dopamine release in the NAc comparable to that observed with addictive substances such as cocaine and opioids. This shared neurochemical response forms the cornerstone of the food addiction hypothesis, suggesting that certain foods can engage reward circuitry with sufficient intensity to produce addiction like behavioural patterns [11,12,13,14,15,16].

The mesolimbic system is highly sensitive to metabolic state, with fasting and food restriction augmenting dopamine system function and increasing the reinforcing value of rewarding stimuli. Conversely, chronic exposure to obesogenic diets and the development of obesity alter dopamine circuit function, affecting not only feeding behaviour but also drug reward and other dopamine-dependent behaviours. These bidirectional interactions between metabolic signals and the mesolimbic dopamine system underscore the complexity of food reward processing and its dysregulation in obesity [13,14,17]

Functional Neuroimaging Findings: Similarities in Brain Activation Patterns

Functional magnetic resonance imaging (fMRI) studies have revealed striking parallels in brain activation patterns between individuals with food addiction and those with substance use disorders. Exposure to food cues in individuals with high food addiction scores elicits elevated activation in reward-encoding regions including the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), amygdala, insula, striatum, and dorsolateral prefrontal cortex (DLPFC), brain areas that similarly show heightened responsivity to drug-related cues in substance-dependent individuals. This hyperactivation reflects enhanced anticipatory reward processing and cue-triggered craving, a phenomenon driven in part by dopamine-mediated incentive salience [12,18,19].

Obese individuals demonstrate increased activation of reward-related brain circuits, particularly the insula and OFC, in response to visual food cues compared to healthy-weight controls, with responses persist even in the satiated state, suggesting impaired satiety signalling and aberrant reward processing. Resting-state fMRI studies further demonstrate that obese individuals exhibit elevated intrinsic activity in the putamen, claustrum, and insula regions involved in habitual control, sensory processing, and interoceptive awareness, independent of food intake. Collectively, these neuroimaging findings support the notion that food addiction shares common neural substrates with drug addiction, involving both cue reactivity and disrupted inhibitory control [12,18,20,21].

Dopamine Receptor Regulation, Tolerance, and Withdrawal in Eating

Chronic consumption of highly palatable foods induces neuroadaptive changes in dopamine receptor expression and function analogous to those observed in substance addiction. Specifically, repeated exposure to rewarding foods leads to downregulation of striatal dopamine D2 receptors (D2R),a phenomenon documented in both obese humans and animal models of diet-induced obesity. This reduction in D2R availability results in decreased sensitivity of the reward system, necessitating increased food intake to achieve equivalent hedonic responses, a hallmark of tolerance. The “reward deficiency syndrome” posits that individuals with lower D2R density experience a blunted reward response, driving compensatory overconsumption of palatable foods and contributing to these maintenance of obesity [14,15,22,23].

The development of tolerance is accompanied by withdrawal-like symptoms when highly palatable foods are restricted or eliminated. Such symptoms include irritability, anxiety, dysphoria, and intense cravings, mirroring the affective and somatic manifestations of drug withdrawal. Animal studies demonstrate that withdrawal from sugar-rich diets produces alterations in mRNA levels of dopamine and opioid receptors similar to those observed during morphine withdrawal. These neuroplastic changes reflect adaptations in both dopaminergic and opioidergic systems, further supporting the biological plausibility of food addiction as a distinct pathological entity [15,24,25,26].

Importantly, the direction of causality between D2R alterations and obesity remains complex. While some that pre-existing low D2R levels may predispose individuals to obesity primarily through reduced energy expenditure and physical activity rather than compulsive eating, other findings indicate that striatal D24 upregulation during critical developmental periods can increase obesity susceptibility via decreased thermogenesis. These findings highlight the multifaceted role of dopamine receptor regulation in both the etiology and maintenance of obesity, emphasizing the need for nuanced therapeutic strategies targeting dopaminergic pathways [27,28].

High-Glycemic Index Carbohydrates and Addictive Like Eating

Glycemic Index, Glycolytic Fluctuations, and Insulin Responses

Glycemic index (GI) quantifies the capacity of a carbohydrate-containing food to raise blood glucose concentration relative to a reference food such as pure glucose or white bread. High-GI foods induce rapid and pronounced elevations in blood glucose, triggering robust pancreatic insulin secretion to restore normoglycemia.  This sequence of hyperglycemia followed by hyperinsulinemia is particularly pronounced after consumption of refined carbohydrates such as white flour, sugar, and potatoes, all of which have undergone processing that removes fiber, protein, and water, thereby accelerating the rate of carbohydrate absorption. Within hours of ingesting a high-GI meal, the exaggerated insulin response can drive blood glucose concentrations below fasting levels, a phenomenon known as reactive hypoglycemia. This postprandial increased hunger, heightened cravings for additional high-GI foods, and a compulsive drive to restore normoglycemia through further consumption, creating a self-perpetuating cycle of overeating [29,30,31,32,33,34].

The pharmacokinetics of high-GI carbohydrates bear striking similarity to those of drugs of abuse, characterized by rapid absorption, swift onset of rewarding effects, and equally rapid clearance that precipitates withdrawal like symptoms. Both glucose and insulin exert direct and indirect modulatory effects on the mesolimbic dopamine system, with glucose signalling to reward centers via the upper intestine and insulin influencing dopamine release in the nucleus accumbens.  This metabolic volatility, the rapid surge and subsequent crash in glucose and insulin is hypothesized to engage addiction related neural circuits with greater intensity than the gradual, sustained energy delivery provided by low-GI, minimally processed foods [12,35,36].

Processed Foods, Rapid Absorption, and Relevance for “Problem Foods”

Ultra-processed foods (UPFs) and highly processed foods (HPFs), typically characterized by elevated content of refined carbohydrates, added sugars, and/or fats, represent the most frequently implicated dietary triggers for addictive like eating behaviours. In a landmark study by Schulte and colleagues, participants rates foods according to their association with addiction like symptoms as operationalized by the Yale Food Addiction scale (YFAS). The higher ranked foods, including chocolate, pizza, French fries, and cake were uniformly highly processed, containing elevated levels of fat and/or refined carbohydrates with high glycemic load (GL). Conversely, minimally processed whole food such as fruits, vegetables, and unprocessed meats were rarely associated with addictive eating patterns [30,37,38].

The addictive potential of these processed foods is attributed to their capacity for rapid delivery of bioavailable rewarding substances, particularly refined carbohydrates that are swiftly absorbed in the proximal intestine where they can maximally stimulate dopamine release in the striatum. Processing techniques strip away structural barriers such as fiber and cell walls that would otherwise slow digestion and absorption, thereby amplifying the speed and magnitude of glucose and insulin excursions. The combination of fat and refined carbohydrates, found in foods such as pizza, ice crea, and baked goods, appears to be particularly potent in activating reward circuitry, with preclinical models demonstrating that foods containing approximately 35% fat and 45% carbohydrate elicit maximal dopaminergic responses and food-seeking behaviour [12,30,31]

Moreover, the early and frequent exposure to UPFs, especially during critical periods of neurodevelopment, may prime the brain’s reward systems for heightened addiction vulnerability across the lifespan. This “gateaway” effect underscores the public health urgency of limiting UPF consumption, particularly among children and adolescents whose developing neural reward pathways are especially susceptible to modification by hyperpalatable, rapidly absorbed foods.

Experimental and Epidemiological Evidence Supporting High-GI Food as Triggers

Experimental evidence from controlled feeding and neuroimaging studies provides compelling support for the role of high-GI carbohydrates in triggering addiction like neural responses. In a randomized, blinded crossover trial by Lennerz and colleagues, 12 overweight or obese men consumed isocaloric, macronutrient- matched meals differing only in GI (high-GI:84% vs low-GI: 37%). Four hours postprandially, a time point critical for influencing subsequent eating behaviour, the high GI meal resulted in lower plasma glucose, greater subjective hunger, and significantly increased cerebral blood flow in the right nucleus accumbens, a key node of mesolimbic reward system. This selective activation of the nucleus, a key node of the mesolimbic reward system. This selective activation of the nucleus accumbens, with an 8.2% relative increase in regional cerebral blood flow, extended to adjacent striatal regions and the olfactory cortex, areas implicated in reward processing, craving, and substance dependence. Importantly, the degree of striatal activation correlated with glycemic and insulinemic responses but not with meal palatability, indicating that metabolic factors rather than taste alone drive the differential neural responses [32,34,39].

Additional neuroimaging studies have demonstrated that individuals with higher food addiction score exhibit exaggerated activation in reward related brain regions and exposed to cues of high-GI, energy dense focus, mirroring the cue reactivity observed in substance use disorders. Preclinical models further corroborate these findings, showing that repeated consumption of high-sugar, high-GI diets induces dopaminergic adaptations, including upregulation of calcium permeably AMPA receptors in the nucleus accumbens, that precede the onset of obesity and are characteristic of addictive substances [12,37].

Epidemiologically, cross-sectional and cohort studies have consistently linked high-GI dietary patterns with increased prevalence of obesity, metabolic syndrome, and type 2 diabetes. Among individuals with obesity, the prevalence of food addiction ranges from 5% to 50%, with significantly elevated rates compared to normal-weight populations. Critically, in a study of adolescent with type 1 diabetes, a population experiencing frequent glycemic fluctuation, 15% met diagnostic criteria for food addiction, and hypoglycemic episodes were significantly associated with higher YFAS symptom scores. These findings suggest that recurrent glucose variability, whether induced by high-GI foods, or metabolic disease, enhances vulnerability to addictive eating by repeatedly activating limbic reward circuits. Collectively, experimental and epidemiological data converge to identify high-GI carbohydrates as potent dietary triggers capable of initiating and sustaining addiction-like eating behaviours, particularly in metabolically vulnerable individuals [12,32,35,40,41,42].

Clinical Phenotypes and Behavioural Manifestations

Intense Cravings, Loss of Control, and Withdrawal When Reducing Intake

The clinical presentation of food addiction is characterized by a constellation of symptoms that parallel those observed in substance use disorders, with intense cravings, loss of control over consumption, and withdrawal-like symptoms representing the most prominent and distressing features. Food cravings defined as powerful, intrusive desires to consume specific food, constitute a central criterion of the food addiction phenotype and have been consistently documented in individuals scoring highly on the Yale Food Addiction Scale (YFAS), as well as in those with binge eating disorder (BED) and bulimia nervosa (BN). These cravings are typically triggered by exposure to food-related cues, including visual, olfactory, or contextual stimuli, and are associated with heightened activation of reward circuitry in the brain, mirroring the cue-induced craving observed in drug addiction. Importantly, food cravings predict poor dieting outcomes and increased likelihood of relapse into maladaptive eating patterns, analogous to the relationship between drug craving and relapse in substance dependence [43,44,45,46].

Loss of control (LOC) over eating represents another hallmark feature, manifesting as the inability to regulate food intake despite conscious intentions to limit consumption. Individuals with food addiction frequently report consuming larger amounts of food than intended, eating over prolonged periods, and experiencing feelings of helplessness or compulsion during eating episodes. This subjective sense of LOC is particularly salient in BED and BN, where it constitutes a diagnostic feature, and has been empirically validated as a core component of the food addiction construct. Among post-bariatric surgery patients, the co-occurrence of LOC eating and food addiction identifies a particularly severe phenotype characterized by elevated eating disorder psychopathology, greater depression, and diminished psychosocial functioning. Nearly 18% of sleeve gastrectomy patients with LOC eating meet criteria for food addiction, underscoring the persistence of addictive eating behaviours even following surgical intervention [44,45,46,47].

Withdrawal symptoms emerge when individuals attempt to reduce or eliminate consumption of specific foods, particularly those high in sugar, fat, and refined carbohydrates. These symptoms include irritability, anxiety, dysphoria, restlessness, fatigue, headaches, and intensified cravings manifestations that closely resemble the affective and somatic withdrawal experienced during cessation of psychoactive substances. The DSM-5 substance use disorder criteria explicitly recognize withdrawal as a key diagnostic feature, and this symptom has been adapted to food addiction with considerable empirical support, although distinguishing genuine withdrawal from energy deficit or psychological reactance to dietary restriction remains a methodological challenge. Animal models further corroborate the existence of food withdrawal, demonstrating neurochemical alterations in dopamine and opioid systems comparable to those observed during drug withdrawal when sugar-rich diets are discontinued [16,26,45].

Overlap with DSM-5 Addiction Criteria

The diagnostic conceptualization of food addiction has been largely derived from the DSM-5 criteria for substance use disorders, with remarkable overlap in symptom profiles. The DSM-5 consolidates 11 criteria for substance use disorders, encompassing impaired control (consuming larger amounts than intended, unsuccessful effort to cut down, time spent obtaining or using, craving), social impairment (failure to fulfil obligations, continues use despite interpersonal problems, activities given up), risky use (use in hazardous situations, continued use despite consequences), and pharmacological criteria (tolerance and withdrawal). Each of these criteria can be translated to eating behaviour with varying degrees of empirical validation [6,45].

The most robustly supported food addiction criteria include: consuming food in larger amounts or over longer periods than intended, persistent desire or unsuccessful efforts to reduce intake, intense craving for specific foods, and continued overeating despite knowledge of physical or psychological harm, all of which have been extensively documented in clinical and non-clinical populations. Tolerance, operationalized as the need for increasing quantities of food to achieve the desired hedonic effect or diminished pleasure from the same amount of food, is biologically plausible given the documented downregulation of dopamine D2 receptors, in obesity and compulsive eating. Withdrawal, as previously discussed, has preliminary support from both human self-report and preclinical studies, though distinguishing it from caloric deprivation remains challenging [43,45].

The YFAS, currently in its second iteration (YFAS 2.0), operationalizes these DSM-5 criteria and classifies food addiction severity as mild (2-3 symptoms), moderate (4-5 symptoms), or severe (≥6 symptoms), provided that clinically significant distress or impairment is present. The YFAS 2.0 has demonstrated strong psychometric properties across diverse populations, including bariatric surgery candidates, individuals with eating disorders, adolescents, and community samples, with internal consistency typically exceeding α = 0.80 and robust convergent validity with measures of binge eating, emotional eating, and eating disorder psychopathology [6,45,47].

Vulnerable Populations and Heterogeneity in Food Addiction Phenotypes

Food addiction exhibits substantial heterogeneity in prevalence, severity, and associated psychopathology across different clinical and demographic populations, reflecting underlying individual vulnerability factors and distinct etiological pathways. Meta-analytic data indicate an overall weighted prevalence of food addiction of approximately 20% in the general population, with significantly elevated rates in clinical samples. Among individuals with eating disorders, prevalence rates are particularly pronounced: 55% in BED, 97.6% in BN, 87.9% in anorexia nervosa binge-eating/purging subtype, and 61.5% in anorexia nervosa restrictive subtype. These differential prevalence rates suggest that food addiction is most strongly associated with disorders characterized by recurrent binge eating and impulsivity rather than dietary restriction alone [48,49,50,51].

Bariatric surgery candidates represent another highly vulnerable population, with food addiction prevalence ranging from 16.5% to 47.4% depending on assessment methods and sample characteristics. Preoperative food addiction in this population is associated with higher levels of binge eating symptoms, depression, anxiety, impulsivity, food cravings, weight and shape concerns, lower quality of life, and diminished eating self-efficacy factors that collectively signal greater eating disorder psychopathology and poorer surgical candidacy. Critically, food addiction status may predict suboptimal weight loss outcomes and increased risk of addiction transfer to substances such as alcohol following bariatric surgery, highlighting the clinical importance of preoperative screening and targeted intervention [53].

Adolescents constitute an underrecognized vulnerable population for food addiction, with prevalence rates of approximately 5% in the general adolescent population and 11.2% among adolescents with a history of mental disorders. The adolescent period represents a critical developmental window characterized by heightened neuroplasticity in reward circuitry, increased susceptibility to impulsivity, and elevated risk for both eating disorders and substance use disorders. Among adolescents with food addiction, higher BMI z-scores, greater emotional and behavioural problems, depression, anxiety, and impaired executive functioning are consistently observed. Early identification and intervention during this critical period may prevent progression to more severe obesity and eating pathology in adulthood [54].

Beyond demographic and clinical categories, food addiction exhibits substantial heterogeneity in underlying psychobiological mechanisms, with emerging evidence supporting the existence of distinct phenotypic clusters defined by co-occurring vulnerabilities. Latent profile analyses have identified subgroups characterized by: low symptom severity with no personality dysfunction (simplex phenotype), high eating disorder symptoms without personality pathology (simplex-severe phenotype), and high eating disorder symptoms with co-occurring dysfunctional personality traits (complex-severe phenotype). The complex-severe phenotype is associated with greater childhood trauma exposure, emotion dysregulation, alexithymia (difficulty identifying and describing emotions), lower interoceptive awareness, and more severe psychiatric comorbidity, including depression, anxiety, and post-traumatic stress disorder (PTSD) [48,55,56,57].

Trauma exposure, particularly childhood maltreatment, emerges as a critical vulnerability factor across multiple studies, with food addiction serving as a maladaptive coping mechanism for emotional distress stemming from early adversity. Women with food addiction exhibit similar levels of PTSD symptoms, depression, and emotion dysregulation as women with substance use disorders, with both groups demonstrating elevated difficulties in impulse control, goal-directed behaviour, and limited access to adaptive emotion regulation strategies compared to individuals without addiction. However, trauma histories differ between the two groups, with substance use disorder associated with more severe childhood and adulthood trauma, suggesting that the intensity and chronicity of trauma exposure may influence whether individuals develop food addiction versus substance addiction [56,58].

Collectively, these findings underscore the clinical heterogeneity of food addiction, with distinct vulnerable populations and phenotypic subtypes that require tailored assessment and intervention strategies. Recognition of this heterogeneity is essential for advancing both the conceptual validity and clinical utility of the food addiction construct, enabling precision medicine approaches that address the specific psychobiological mechanisms driving addictive-like eating in individual patients [12,48].

Food Addiction and the Obesity Epidemic

How Addiction-like Behaviours Drive Excessive Caloric Intake

Food addiction represents a critical etiological factor contributing to the global obesity epidemic, with accumulating evidence demonstrating that addiction-like behaviours toward highly palatable foods directly promote excessive caloric intake beyond metabolic needs. In a landmark population-based study of 652 adults, the prevalence of food addiction was 5.4% overall, with significantly higher rates among women (6.7%) than men (3.0%), and prevalence increased progressively with obesity status. Critically, individuals meeting criteria for food addiction weighed on average 11.7 kg more, had 4.6 higher BMI units, and carried 8.2% greater body fat and 8.5% more trunk fat compared to non-food-addicted individuals, even after controlling for confounding variables including age, sex, medication use, physical activity, and smoking. Moreover, 80-88.6% of food-addicted individuals were classified as overweight or obese, providing compelling evidence that food addiction substantially contributes to the rising prevalence of obesity in the general population [59].

The mechanistic pathways through which food addiction drives overconsumption involve dysregulation of both homeostatic and hedonic eating systems. Homeostatic eating is governed by metabolic signals including leptin, ghrelin, and insulin that coordinate energy balance, whereas hedonic eating is driven by the rewarding properties of food consumption mediated by mesolimbic dopamine circuits, independent of caloric need. In individuals with food addiction, hedonic mechanisms override homeostatic satiety signals, resulting in persistent food-seeking and consumption despite physiological repletion. This dissociation between metabolic state and eating behaviour is particularly pronounced in response to food cues like visual, olfactory, or contextual stimuli associated with palatable foods which trigger intense cravings and compulsive consumption even in the absence of hunger [60,61,62].

Neuroimaging studies demonstrate that obese individuals exhibit hyperactivation of reward-related brain regions, including the nucleus accumbens, orbitofrontal cortex, amygdala, and ventral pallidum, upon exposure to food cues or palatable food consumption compared to lean controls. This heightened cue reactivity predicts subsequent weight gain and reflects enhanced motivational salience attributed to food stimuli, a process mediated by dopaminergic signalling that parallels drug cue reactivity in substance use disorders. Importantly, this hyperresponsivity of reward circuitry persists across repeated exposures, driving habitual, automatic eating behaviours that become increasingly resistant to conscious inhibitory control [60,62].

The addictive properties of specific food categories further compound excessive intake. Ultra-processed foods characterized by high glycemic index, added sugars, refined fats, and salt are preferentially associated with addiction-like eating patterns and account for a disproportionate share of total caloric intake in Western diets. These foods trigger rapid dopamine release in the striatum, reinforcing consumption through positive hedonic feedback, while their rapid absorption kinetics produce volatile glucose-insulin oscillations that perpetuate craving-consumption cycles. Consequently, individuals with food addiction consume larger quantities of energy-dense foods at higher frequency, with diminished dietary diversity and reduced intake of nutrient-dense whole foods, dietary patterns strongly predictive of weight gain and metabolic disease[59,63].

Neuroadaptation, Reward Deficiency, and Overeating in Obesity

Chronic overconsumption of highly palatable foods induces neuroadaptive changes in reward circuitry that perpetuate overeating and obesity through mechanisms analogous to those observed in drug addiction. Central to this process is the phenomenon of reward deficiency syndrome (RDS), a construct positing that genetic polymorphisms and epigenetic modifications affecting dopamine receptor expression and signalling result in hypo-dopaminergic function and blunted reward sensitivity. Individuals with RDS experience diminished pleasure from natural rewards, driving compensatory overconsumption of highly rewarding stimuli like drugs in the case of substance addiction, and palatable food in the case of obesity to transiently restore reward circuit activity [30,31,37,45].

The neurochemical hallmark of RDS in obesity is reduced striatal dopamine D2 receptor (D2R) availability, a finding consistently replicated across multiple positron emission tomography (PET) studies. Wang and colleagues first demonstrated that pathologically obese individuals exhibit significant reductions in striatal D2R density comparable to those observed in cocaine- and alcohol-dependent individuals, with D2R availability inversely correlated with body mass index. This reduction in D2R density is associated with decreased sensitivity of dopamine-regulated reward circuits, necessitating increased food intake to achieve equivalent hedonic responses, the neurobiological equivalent of tolerance. Prospective studies further reveal that individuals carrying the DRD2 Taq1A A1 allele, a genetic variant associated with approximately 30% reduced striatal D2R expression, exhibit blunted reward region responsivity to palatable food and significantly greater weight gain over one-year follow-up compared to non-carriers [64].

Critically, the relationship between D2R availability and obesity appears bidirectional, reflecting both genetic predisposition and neuroplastic consequences of chronic overeating. Animal studies demonstrate that assignment to overfeeding versus non-overfeeding conditions results in rapid downregulation of D2R availability, reduced dopamine turnover, and diminished responsivity of reward regions to food intake, drug administration, and electrical brain stimulation. These findings support a dynamic vulnerability model in which initial hyper-responsivity of reward circuits to palatable food promotes overeating, leading to compensatory downregulation of D2R density and dopamine signalling, which in turn drives further compulsive consumption to overcome the blunted reward response, a feed-forward cycle that accelerates weight gain and entrenches addictive eating behaviours [62].

Beyond dopaminergic systems, endogenous opioid receptors (EORs), particularly mu-opioid receptors (MORs), play a critical role in mediating the hedonic value of palatable food and contribute to reward deficiency in obesity. PET imaging studies reveal that individuals with obesity exhibit reduced MOR availability in the nucleus accumbens compared to healthy-weight controls, paralleling findings in substance use disorders. Animal models corroborate this observation, showing decreased MOR mRNA expression in the nucleus accumbens of obesity-prone rats exposed to high-fat diets. Conversely, pharmacological activation of MORs in the nucleus accumbens potently stimulates consumption of high-calorie foods, suggesting that diminished opioidergic tone may paradoxically drive compensatory overeating in an attempt to restore hedonic homeostasis. The convergence of dopaminergic and opioidergic deficits in obesity underscores the multifaceted nature of reward deficiency and highlights the need for therapeutic strategies targeting multiple neuromodulatory systems [64].

Neuroadaptations in obesity extend beyond receptor expression to encompass structural and functional remodelling of cortical regions involved in executive control and decision-making. Obese individuals demonstrate reduced activation of the dorsolateral prefrontal cortex (dlPFC), a region critical for inhibitory control and goal-directed behaviour, in response to food cues and during cognitive tasks requiring self-regulation. This hypofrontality contributes to impaired impulse control, diminished ability to delay gratification, and increased susceptibility to cue-triggered eating, behavioral phenotypes characteristic of both obesity and addiction. Conversely, individuals who successfully maintain weight loss exhibit enhanced dlPFC activation and greater dietary restraint, suggesting that strengthening prefrontal executive function represents a viable target for obesity interventions [60].

Obesity as a Phenotype of Chronic Maladaptive Food Reward

The conceptualization of obesity as a phenotype of chronic maladaptive food reward integrates genetic vulnerability, environmental exposure, and neuroplastic adaptations into a unified framework that parallels contemporary models of addiction. In this model, initial exposure to obesogenic environments characterized by ubiquitous availability of ultra-processed, hyper-palatable foods engages reward circuitry, triggering dopamine and opioid release that reinforces consumption. In genetically susceptible individuals, those carrying risk alleles affecting dopamine and opioid receptor function, or exhibiting baseline reward deficiency, this hedonic feedback is particularly salient, driving repeated consumption that exceeds homeostatic requirements [62,65].

As consumption patterns become habitual, neuroadaptive processes emerge, including downregulation of D2R and MOR, reduced dopamine synthesis and turnover, and diminished functional connectivity within cortico-striatal-limbic circuits. These adaptations collectively attenuate reward sensitivity, establishing a state of chronic reward deficiency that perpetuates compulsive food-seeking analogous to the “dark side” of addiction described in substance use disorders. Simultaneously, the excitatory transmission within the basal ganglia is enhanced, mirroring the neuroplastic changes observed with chronic drug exposure, which further skews valuation processes and transforms food stimuli into hyper-salient motivational cues. This remodelling of valuation circuitry imbues food cues with exaggerated incentive salience, driving persistent craving and food-seeking despite adverse metabolic, physical, and psychosocial consequences [13,62,65].

The maladaptive reward phenotype in obesity is further reinforced by epigenetic mechanisms that alter gene expression in reward-related circuits. Chronic exposure to high-fat, high-sugar diets during critical developmental periods, particularly childhood and adolescence, induces epigenetic modifications, including DNA methylation and histone acetylation that persistently dysregulate dopamine signalling and executive function. Obese children exhibit higher activation of reward regions and blunted post-meal deactivation of the prefrontal cortex and nucleus accumbens, suggesting early-life establishment of abnormal food motivation circuitry that predisposes to lifelong obesity. These neurodevelopmental trajectories underscore the importance of primary prevention strategies targeting dietary exposures during vulnerable periods of brain maturation [62].

Importantly, the maladaptive food reward phenotype in obesity exhibits considerable heterogeneity, with distinct subgroups characterized by varying degrees of reward hyper-responsivity versus reward deficiency. Some individuals display enhanced constitutive responsiveness of reward systems that drives initial overconsumption and weight gain, whereas others exhibit primary reward deficiency stemming from genetic variants that predispose to compensatory eating. Over time, these initially distinct phenotypes may converge as chronic overconsumption induces reward deficiency even in individuals with initially intact reward function, illustrating the dynamic, reciprocal interactions between behaviour, environment, and neurobiology in the pathogenesis of obesity [62].

Finally, the concept of obesity as a chronic maladaptive reward phenotype has profound implications for intervention and relapse prevention. Caloric restriction and dieting, while essential for weight loss, paradoxically exacerbate reward deficiency by further reducing dopamine signalling and reward region responsivity, increasing vulnerability to relapse into compulsive eating behaviours. This neurobiological reality accounts for the notoriously high failure rates of conventional dietary interventions and underscores the necessity of adjunctive strategies, including pharmacological dopamine agonism, cognitive-behavioural interventions to enhance executive control, and environmental restructuring to minimize cue exposure that address the underlying reward circuit dysfunction driving obesity [62,65].

Interventions, Controversies, and Future Directions

Implications for Prevention and Clinical Management

Prevention and management of food addiction represent critical challenges for metabolic health interventions, requiring multidimensional strategies that integrate nutritional, behavioural, and technological approaches. Evidence from cohort and clinical studies supports therapeutic carbohydrate reduction (TCR), combined with behavioural coaching and structured dietary programs, as a core intervention that can produce substantial improvements in food addiction and binge eating symptoms. Telemedicine, text-based communication, wellness coaching, asynchronous education, and real-time biofeedback in digital health platforms have shown significant reductions in food addiction severity, sometimes equalling pharmacotherapy but with fewer adverse effects and better long-term sustainability. Nutritional strategies that emphasize exclusion of known trigger foods, such as high-glycemic-index and ultra-processed foods may improve dietary adherence and metabolic outcomes, while promoting emotional regulation and restoring self-efficacy. Adjunctive therapies may include cognitive behavioural therapy (CBT), mindfulness-based interventions, and peer support, each shown to modulate addictive eating patterns and improve self-regulation [43,68].

Current Controversies in The Diagnosis and Treatment of Food Addiction

The diagnosis and nosological status of food addiction remain the subject of significant controversy within both clinical and research communities. Central debates concern whether food addiction is best viewed as a substance-related disorder (with specific foods acting as triggers) or a behavioural disorder (driven by maladaptive patterns around eating), and whether it represents a distinct entity or shares etiological overlap with obesity and established eating disorders such as binge eating disorder (BED) or bulimia nervosa. The use of diagnostic scales such as the Yale Food Addiction Scale (YFAS) has provided some standardization but is criticized for difficulties distinguishing pathological food addiction from strong but normative food preferences, as well as for its restrictive DSM criteria-based perspective that may not fully capture the range of eating pathology. Furthermore, it is neither feasible nor desirable to prescribe complete abstinence from food as with substance addiction, complicating therapeutic goals and relapse prevention strategies. Treatment guidelines remain unstandardized, and pharmacologic interventions such as stimulant and GLP-1 receptor agonists have shown only moderate efficacy with risk of side effects and limited long-term adherence [43,69].

The Need for Novel Therapeutic and Policy Strategies

The complex and multifactorial nature of food addiction points to the urgent need for innovative, evidence-based therapeutic and policy solutions. Clinical management must move beyond calorie restriction alone to address reward, motivational, and self-regulation systems underlying addictive eating, applying insights from addiction science including new pharmacotherapies, personalized psychotherapies, and neuromodulation strategies. Cross-disciplinary collaboration is essential; interventions should be tailored to individual patient profiles considering genetics, upbringing, social determinants, trauma history, and neurobiology. On a population level, policies aimed at reducing exposure and access to ultra-processed food environments through reformulation, marketing restrictions, labelling, and taxation can help curtail addictive eating drivers and improve public health outcomes. Continued research, especially head-to-head comparisons of behavioural, dietary, and pharmacological interventions, is needed to develop patient-centered approaches and clarify the biological and social dimensions of food addiction as both a clinical and societal concern [12,70].

Conclusion

Food addiction has emerged as a compelling neurobiological and clinical construct that fundamentally reshapes our understanding of the modern obesity crisis. Evidence from clinical, neuroimaging, and epidemiological studies demonstrates that addiction like eating behaviours marked by intense cravings, loss of control, and withdrawal, actively drive excessive caloric intake, particularly in response to ultra-processed, high-glycemic index (GI) foods. These foods uniquely hijack brain reward circuits, reinforce dysregulated eating patterns, and foster maladaptive neuroplastic changes, leading to chronic overconsumption and metabolic dysfunction.

The central role of high-GI carbohydrates in contemporary addiction biology stems from their pharmacokinetic profile: rapid absorption triggers acute surges in blood glucose and insulin, followed by population studies converge to show that frequent exposure to these rapidly absorbed carbohydrates primes neural reward pathways, enhances craving, and increases the prevalence of food addiction and obesity, especially in metabolically vulnerable individuals, such a s those with histories of trauma, psychiatric comorbidities, or genetic predispositions.

Addressing food addiction and its contribution to the obesity epidemic requires bold, multi-level, evidence-based strategies. Prevention and treatment must move beyond simple calorie restriction to include personalized nutrition interventions, behavioural therapies, technological supports, and policy reforms. These should target both biological vulnerabilities, such as reward deficiency and executive function deficits, as well as environmental drivers, including the ubiquitous availability and marketing of addictive food products. Population level public health policies restricting ultra processed food access, promoting food environment reformulation, and investing in multidisciplinary clinical research are essential to reduce the burden of food addiction and foster long-term metabolic health.

Ultimately, integrating neurobiological insights and addiction science into the prevention and management of obesity is paramount. The adoption of multi-disciplinary approaches will be crucial in reversing the trajectory of this crisis and ensuring that treatment is both patient-centered and grounded in the latest evidence for effective metabolic health promotion.

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