Prefrontal cortex immaturity and reward circuit hijacking: Why anti-obesity policies fail to protect children from ultra-processed food overconsumption

Abstract

The prevalence of obesity in pediatric populations has reached epidemic levels, largely due to consumption of ultra-processed foods (UPFs), whose formulations are optimized for hyperpalatability and promote overconsumption in children and adolescents due to neurodevelopmental vulnerabilities. The prefrontal cortex, which governs planning, decision-making, and impulse control, reaches full maturity around 25 years of age. Children and adolescents have limited self-regulatory capacity, as their reward circuitry responds excessively to palatable stimuli. The high palatability and marketing of UPFs may interact with this neurobiological imbalance, triggering dopamine release and promoting addictive-like eating behaviors. Despite public health interventions such as front-of-package labeling, nutrient-based taxes, and restrictions on child-targeted marketing, evidence suggests these measures have had modest impact on consumption patterns. We hypothesize that the limited success of these approaches may be explained by their failure to address the underlying neurobiological mechanisms driving excessive consumption. Therefore, a paradigm shift toward parental education programs that foster healthy home food environments and promote early self-regulation skills is warranted, combined with family-based behavioral treatment. Finally, the potential role of pharmacological agents (e.g., glucagon-like peptide-1 agonists) that target the reward system in cases of severe pediatric compulsive overconsumption warrants future research, given the limited safety data in children.

Key Words: Childhood obesity; Ultra-processed foods; Food addiction; Prefrontal cortex; Reward system; Public health policy; Parental education; Family-based therapy

Core Tip: The obesity epidemic in the pediatric population has been linked to the overconsumption of ultra-processed foods, whose hyper-palatability stimulates reward and disrupts the balance between the immature prefrontal cortex and the overactive reward circuitry during neurodevelopment. Current regulatory measures such as front-of-pack labeling, nutrition-based taxation and advertising restrictions have shown disappointing results in decreasing pediatric obesity. We propose a paradigm shift by giving parents education programs, developing early self-regulation skills in children, implementing cognitive behavioral and family-based therapies, and carefully evaluating dopamine-targeted pharmacological agents as a potential future option for severe, treatment-refractory cases, given limited long-term safety data in children.

INTRODUCTION

Obesity is a complex chronic disease characterized by the abnormal accumulation of adipose tissue and involves genetic, biological, environmental, socioeconomic, and cultural factors, with prominent neurometabolic components, including dysregulation of energy homeostasis, appetite control, and reward processing[1-3]. Obesity develops through an imbalance between energy intake and energy expenditure and is associated with neuroendocrine, inflammatory, and behavioral alterations that affect multiple systems responsible for regulating energy balance, including the gut–brain axis. These systems collectively modulate energy homeostasis and may promote the accumulation of adiposity[4].

Childhood obesity is one of the most concerning public health challenges worldwide because of its rapidly increasing prevalence and its long-term health consequences. In 2024, more than 35 million children under 5 years of age were overweight, and the prevalence of overweight or obesity among individuals aged 5-19 years increased from 8% in 1990 to 20% in 2022. Similarly, the number of children with obesity rose from approximately 31 million to more than 160 million during the same period[5]. These trends have led to the recognition of childhood obesity as a global health crisis and reflect substantial limitations in current prevention strategies[6]. Therefore, childhood obesity should be examined from a multifactorial perspective that considers the determinants contributing to its development and persistence. One of the most well-established contributors is a dietary pattern characterized by excessive intake of energy-dense, nutrient-poor foods, combined with sedentary behaviors[1,3]. However, the World Health Organization has emphasized that the rapid global increase in childhood obesity cannot be explained solely by individual behaviors, but also by broader changes in social structures and food environments[5].

In addition to obesity, type 2 diabetes (T2D) is one of the most concerning conditions in the pediatric population, as it was previously considered rare in children. Over the past two decades, its incidence has increased steadily, particularly among children with obesity, a family history of the disease, and prolonged exposure to high-calorie diets[7]. This trend may be partly attributable to the rise in childhood obesity described in the previous paragraph, given that obesity can increase the risk of developing T2D up to fourfold[8,9]. The coexistence of obesity and T2D during childhood substantially increases the risk of subsequent cardiometabolic diseases, underscoring the urgency of implementing early obesity prevention and management strategies using innovative approaches[10-12].

The global increase in childhood obesity has been associated with a dietary transition toward increased consumption of ultra-processed foods (UPFs), which are highly refined industrial formulations composed primarily of processed ingredients and additives and contain elevated amounts of sugar, fat, sodium, and dietary emulsifiers. These products are specifically engineered for hyperpalatability[13-16]. This nutritional shift has been driven by sociocultural changes that favor convenience over nutritional quality and have consolidated UPFs as predominant components of modern food systems[14,16]. These dietary patterns may promote overeating and obesity by disrupting energy homeostasis through multiple pathways, including the brain reward circuitry and appetite regulation[15,17].

Growing evidence linking excessive consumption of UPFs to adverse health outcomes has reinforced the perception that public health strategies targeting the food environment are necessary, including fiscal measures, front-of-package (FOP) labeling, and advertising regulations to reduce the consumption of these products[15]. In addition, the need to promote minimally processed whole foods and to implement nutrition education programs in schools has been emphasized, despite persistent challenges related to unequal access to healthy foods, industry influence, and behavioral barriers to dietary change[14,18]. However, the continued increase in the prevalence of obesity and T2D in the pediatric population raises concerns about the effectiveness of prevention policies that focus primarily on education and individual responsibility without accounting for the neurodevelopmental vulnerabilities of children and the influence of the contemporary food environment. Therefore, this issue should be examined from a neuroevolutionary perspective.

In this context, it has been suggested that dietary patterns that promote weight gain reflect eating behaviors driven by the pursuit of immediate gratification rather than by nutritional requirements. This process is mediated by the brain reward circuitry, a complex network centered on the mesolimbic dopaminergic pathway. This pathway extends from the ventral tegmental area (VTA) to the nucleus accumbens (NAc) and the prefrontal cortex (PFC) and is modulated by interconnected brain regions, neurotransmitter systems, and peripheral signals (Figure 1). This circuitry processes rewarding stimuli, mediates motivation and reinforcement, and represents a primary target of addiction-related neuroadaptations[19-21]. High intake of UPFs has been associated with altered patterns of brain activation and structural changes in regions involved in appetite regulation and reward processing[22]. This issue is particularly relevant in the pediatric population, as the reward circuitry may be especially vulnerable during critical stages of neurodevelopment. Such vulnerability may contribute to impaired control of food intake and increase the risk of cardiometabolic diseases at an early age[13]. Although evidence regarding altered reward circuitry functioning in children with overweight remains limited, several studies suggest potential alterations in brain connectivity that support this hypothesis[23].

Figure 1 Schematic representation of reward circuitry activation induced by ultra-processed foods. Ingestion of ultra-processed foods (UPFs), stimulates gustatory receptors in the oral cavity. Sensory signals are transmitted primarily via the facial (VII), glossopharyngeal (IX), and vagus (X) cranial nerves. These gustatory afferents converge in the hypothalamus (dotted lines), from where the pathway activates dopaminergic neurons in the ventral tegmental area. Dopaminergic projections (orange arrows) subsequently release dopamine in the nucleus accumbens (mediating immediate hedonic pleasure), the amygdala (encoding emotional valence), and the prefrontal cortex (supporting executive control and value-based decision-making). This neurocircuitry underlies the potent motivational and reinforcing effects of UPFs.

On this basis, we review the functioning of the reward circuitry and its role in the dysregulated consumption of UPFs. Next, we examine how neurodevelopmental vulnerabilities in children and adolescents may enhance the hedonic intake of UPFs. We also analyze why public policies, including FOP labeling, nutrient-based taxation, and restrictions on child-targeted marketing, have had a limited effect on reducing UPF consumption among children and adolescents. Accordingly, we propose that improved outcomes may be achieved through parental education strategies, the development of self-regulation skills, and psychological interventions. Finally, we examine the potential for pharmacological modulation of the reward circuitry, particularly through the management of comorbidities associated with binge eating disorder. We propose that a comprehensive approach addressing these dimensions simultaneously may be more effective in reducing excessive UPF consumption and its cardiometabolic consequences by promoting improved regulation of the reward circuitry in children.

LITERATURE SEARCH AND REVIEW METHODOLOGY

A narrative review was conducted. The literature search included combinations of the following keywords: “adolescent brain development”, “prefrontal cortex maturation”, “reward circuitry”, “ultra-processed foods”, “food addiction”, “compulsive food overconsumption”, “psychological therapy”, “pharmacological therapy”, and “public health policy”. Only articles published between 2000 and 2026 were included. The search was performed using PubMed, Scopus, Web of Science, and Google Scholar. The types of articles included in the analysis comprised original research articles, narrative reviews, systematic reviews, and meta-analyses. Only peer-reviewed articles published in English were included. Articles published in journals that do not adhere to rigorous peer-review standards, those written in languages other than English, those not indexed in the aforementioned databases, and retracted articles were excluded.

NEUROBIOLOGICAL MECHANISMS OF COMPULSIVE UPF OVERCONSUMPTION

In this section, we analyze the role of the dopaminergic reward circuitry in compulsive UPF overconsumption to provide context for how vulnerabilities in this system during childhood and adolescent neurodevelopment may increase susceptibility to excessive UPF intake.

When consuming a UPF, taste receptors in the papillae of the tongue and oral cavity are activated, sending signals via cranial nerves VII (facial), IX (glossopharyngeal), and X (vagus) to the nucleus of the solitary tract in the brainstem. From there, these signals are projected to the insular cortex, where conscious perception of taste is generated, and to limbic regions that activate the hypothalamus and subsequently the VTA[24-26] (Figure 1). This activation stimulates dopaminergic neurons in the VTA to release substantial amounts of dopamine into the NAc, generating an immediate sensation of pleasure[27-29]. Released dopamine then spreads through dopaminergic projections to other structures within the reward circuitry, where it exerts distinct effects. In the amygdala, it contributes to the formation of intense emotional memories linking food with pleasure. In the PFC, it facilitates conscious planning to repeat the behavior[30-32]. Conversely, chronic exposure to elevated dopamine levels within the reward circuitry induces neuroadaptations associated with tolerance, including hypoactivity of the PFC and reductions in gray matter volume. These changes may diminish executive control and rational planning, thereby promoting a behavioral shift from voluntary to compulsive and impulsive patterns, particularly in contexts of early and culturally normalized exposure to UPFs[33-36]. This neuroadaptive transition is further reinforced by the amygdala, which encodes emotionally salient reward memories and can reactivate cravings during stress, potentially contributing to a self-perpetuating cycle[36,37].

The amygdala plays a crucial role in reinforcing addictive cycles associated with UPF consumption, particularly in response to everyday stress, anxiety, or negative emotional states. This brain structure reactivates pleasurable memories linked to the rewarding effects of these foods, thereby generating intense cravings. These cravings can automatically drive repeated consumption as a form of temporary relief from negative emotional states. This process creates a self-perpetuating cycle in which individuals repeatedly seek these highly palatable foods to alleviate stress or discomfort, thereby reinforcing maladaptive behaviors and contributing to the compulsive nature of UPF consumption (Figure 2). Neurobiological research indicates that tolerance and withdrawal phenomena engage brain stress systems within extended amygdala circuits, thereby contributing to negative emotional states during abstinence and increasing the drive to consume UPFs[37-39]. Although most mechanistic insights are derived from rodent models of palatable food exposure, which allow causal inference, human neuroimaging and epidemiological studies are predominantly cross-sectional or short-term longitudinal. Therefore, these associations should be interpreted cautiously, and prospective study designs are warranted.

Figure 2 Vicious cycle of ultra-processed foods consumption in children and adolescents. The diagram illustrates a self-perpetuating neurobehavioral loop initiated by: A: Anticipation or visual/olfactory exposure to ultra-processed foods, which elicits anticipatory happiness and craving via amygdala activation; B: Ingestion activates gustatory (cranial nerves VII, IX, X) and post-ingestive (gut-brain) reward pathways; C: Massive dopamine release in the NAc, amygdala, and prefrontal cortex produces intense hedonic pleasure and forms strong emotional memories; D: Subsequent everyday stress, anxiety, or negative affect reactivates the cycle via amygdala-driven cravings. This loop is exacerbated by prefrontal immaturity and contributes to compulsive overeating despite known health consequences.

NEURODEVELOPMENTAL VULNERABILITIES IN CHILDHOOD AND ADOLESCENCE

Neurodevelopment is a nonlinear process influenced by multiple factors that can affect the functioning of the reward circuitry. During the first years of life, brain architecture is dynamically shaped by sensory, social, and emotional experiences, capitalizing on heightened neural plasticity to establish foundational representations of the self and the environment[40].

Maturation progresses regionally, beginning in the primary sensory areas and extending to higher-order regions such as the PFC, which undergoes substantial development throughout adolescence and does not reach full structural and functional maturity until approximately 25 years of age[41,42]. Recent longitudinal evidence indicates that prefrontal gray matter thinning and white matter maturation continue into the mid-20s, following a sensorimotor-to-association axis in which higher-order association areas, including the PFC, exhibit more prolonged plasticity than sensorimotor regions[43]. Protecting children from adverse experiences is essential, as neuroimaging evidence in youth demonstrates that early exposure to stimuli such as violence is associated with altered brain development, including reduced medial PFC volume[44]. This issue is particularly important because the PFC is a central component of the neural reward circuitry and plays a critical role in regulating consumption and executive control. Therefore, disturbances in its development may contribute to increased compulsivity and addictive-like consumption patterns by disrupting reward processing and inhibitory control mechanisms[37].

However, adolescence is characterized as a transitional stage between childhood and adulthood and is marked by the onset of puberty, which involves changes in social functioning and cognitive capacity, as well as substantial neurological development[45]. The temporal convergence of heightened plasticity in association cortices, incomplete cognitive control, and hyperactivity of the reward circuitry renders late childhood and adolescence critical developmental periods that are highly sensitive to environmental influences[46]. During adolescence, the PFC continues to undergo prolonged structural and functional maturation, including a progressive reduction in gray matter in regions such as the dorsolateral PFC[47] and an increase in white matter associated with myelination and strengthening of frontostriatal connectivity. This neural reorganization coincides with increased sensation-seeking behavior and reward hypersensitivity, which may be exacerbated by abrupt increases in dopamine levels within the NAc[48]. Reward hypersensitivity is further amplified by the nonlinear trajectory of prefrontal development, characterized by a peak in gamma oscillatory and spiking activity during early adolescence, followed by microglia-mediated circuit refinement in late adolescence[49]. This dynamic reorganization appears critical for the emergence of adult-like cognitive control and may help explain why adolescence represents a period of both heightened vulnerability and opportunity for behavioral change.

Additionally, reduced efficiency of frontal inhibitory control circuits within the PFC has been described, impairing the regulation of reward-related impulses. During adolescence, incomplete maturation of these prefrontal regions limits the ability to inhibit consumption behaviors in the presence of highly reinforcing stimuli, thereby favoring compulsivity[50]. Therefore, an imbalance characterized by heightened incentive responses within the dopaminergic pathway and diminished prefrontal inhibitory control may create a vulnerability profile for behavioral patterns associated with UPF overconsumption. This imbalance between reward-driven motivation and immature prefrontal regulation is consistent with recent models proposing that adolescence is characterized by prolonged plasticity in association cortices, which, although adaptive for learning, also increases susceptibility to environmental influences such as highly palatable foods[43,49].

REWARD CIRCUIT HIJACKING BY UPFs IN CHILDREN AND ADOLESCENTS

Building upon the neurodevelopmental vulnerabilities outlined in the previous section, namely the prolonged maturation of the PFC and the heightened reactivity of the reward circuitry during childhood and adolescence, this section explores the resulting imbalance that may predispose young individuals to compulsive UPF overconsumption[13].

Reward circuit hijacking refers to a cascade of well-documented neuroadaptive processes triggered by repeated exposure to the hyper-rewarding properties of UPFs. These processes include long-term potentiation and synaptic plasticity in the NAc that strengthen cue–reward associations; downregulation of striatal dopamine D2 receptors, leading to reduced reward sensitivity (tolerance); a progressive shift from goal-directed to habitual and compulsive seeking behavior; and recruitment of stress systems within the extended amygdala that drive negative reinforcement during abstinence[35,38].

In children and adolescents with developing taste preferences, exposure to UPFs, combined with genetic predispositions, traditional practices, and obesogenic environments, may shape lifelong unhealthy and addictive-like eating behaviors driven by immature cognitive control and enhanced reward processing, as the still-developing PFC exhibits deficits that impair inhibition and foresight. This may contribute to overeating and disruption of reward neurocircuitry and neural plasticity[51-53]. Neuroimaging evidence indicates that, in response to rewarding stimuli, adolescents exhibit exaggerated activation in reward-related regions such as the NAc. These activation levels resemble those observed in adults, although their magnitude is greater. Meanwhile, PFC engagement remains immature and less focal[54]. Furthermore, a reduced striatal response to food receipt is associated with both current obesity and future weight gain, particularly in individuals carrying genetic variants that reduce dopamine signaling (e.g., the TaqIA A1 allele), suggesting that overeating may represent a compensatory response to an underactive reward circuitry[55]. This may create a feedback loop, as shown in Figure 2, whereby the initial consumption of UPFs produces intense pleasure that reinforces the behavior through associative learning[13]. This pattern is illustrated by a study in which obese rats with unrestricted access to palatable food repeatedly consumed excessive amounts, resulting in progressively worsening deficits in neural reward responses, including desensitization or hypofunction of the reward circuitry, downregulation of striatal dopamine D2 receptors, and the emergence of compulsive-like feeding behavior. This phenomenon is characterized by the need to increase intake to achieve comparable satisfaction, similar to the tolerance observed in drug addiction[35].

Furthermore, deficits in emotional regulation may exacerbate this cycle. Stress or negative emotional states, which are common in young people, can intensify the drive for rewarding stimuli as a coping mechanism, with UPFs acting as readily available “comfort foods”. Greater cumulative exposure to stressors across the lifespan may enhance the negative reinforcement of stress-related snacking, thereby strengthening the association between stress and UPF overconsumption[56,57]. This overreliance on UPFs as a strategy for stress and emotion regulation may establish a foundation for persistent overeating behaviors that extend beyond immediate coping and potentially lead to long-term disruptions in eating patterns. As demonstrated in longitudinal data from the Avon Longitudinal Study of Parents and Children, persistent or increasing childhood overeating is associated with a significantly higher likelihood of binge eating and binge-eating disorder during adolescence. This finding emphasizes the continuity of eating behaviors that may evolve into disordered patterns and persist into adulthood if left unaddressed[58].

Parallels between compulsive UPF overconsumption and substance addiction models

Although chronic exposure to UPFs initially triggers enhanced dopamine release and heightened pleasure, over time it leads to mild downregulation of striatal D2 dopamine receptors and dysregulation of satiety hormones, including ghrelin and leptin. Importantly, the term “UPF addiction” is not synonymous with the broader and still-debated construct of “food addiction”. “UPF addiction” is used to emphasize the hyperpalatability and specific formulation of UPFs that uniquely exploit reward circuitry[59]. Both concepts remain outside formal Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5) diagnoses and continue to be subjects of scientific debate. This process is analogous to early neuroadaptive changes observed in obesity and substance addiction[13,59,60]. It may create a dependency cycle in which increasing consumption is required to achieve the same level of reward, thereby perpetuating compulsive overeating[39,17]. Animal models provide supporting evidence: Rats fed diets designed to mimic UPFs exhibit compulsive-like feeding despite adverse consequences, driven by elevated dopamine levels in the NAc[61].

The addictive potential of UPFs in young people shares similarities with substance use disorders, as both involve dysregulation of the reward circuitry[59]. Key DSM-5 criteria for substance use disorders, including loss of control, tolerance, withdrawal, and continued use despite negative consequences, have been observed in individuals exhibiting addictive-like eating behaviors, particularly among adolescents with obesity[62,63]. For example, the Yale Food Addiction Scale for Children (YFAS-C), which is based on substance use disorder diagnostic criteria, has identified addictive-like eating behaviors in approximately 12%-15% of children and adolescents in recent meta-analyses. These behaviors overlap with those observed in nicotine or alcohol dependence[64].

Neurobiologically, UPFs and drugs of abuse converge on the reward circuitry, where both induce supraphysiological dopamine release[44]. Preclinical evidence indicates that sugar alone can produce behavioral sensitization and cross-tolerance with amphetamines, suggesting shared neurobiological mechanisms[65]. Similar to the way in which early substance exposure increases the risk of lifelong addiction, habitual UPF consumption may alter reward circuitry and potentially increase the risk of comorbid conditions such as depression or substance misuse[13]. Additionally, chronic exposure to UPFs has been shown to trigger neuroadaptations that reduce reward sensitivity and perpetuate compulsive behavior in the context of negative emotional states[66]. Epidemiological studies further support this association, linking childhood obesity to an increased risk of developing a substance use disorder later in life. This evidence underscores the importance of approaching compulsive UPF overconsumption from the perspective of addiction medicine[67].

In summary, the imbalance between reward sensitivity and impulse control, in conjunction with neurodevelopmental factors, renders children and adolescents particularly susceptible to compulsive UPF overconsumption. The complexity of this phenomenon helps explain why interventions such as individual dietary counseling, exercise prescriptions, and educational campaigns promoting balanced eating often fail to achieve the expected reductions in UPF consumption.

CURRENT PUBLIC HEALTH POLICIES FOR LIMITING UPFs AND THEIR LIMITATIONS

The impact of food palatability and marketing on pediatric populations

The engineered palatability of UPFs amplifies their impact on vulnerable youth, particularly when combined with industry-driven promotion and consumer appeal[13,68]. This potent combination of engineered hyperpalatability and targeted marketing creates a powerful neurobehavioral dynamic that capitalizes on the immature PFC of children, thereby making self-regulation more challenging[68,69]. Palatability optimized through “bliss point” formulations of salt, sugar, fat, and enhanced texture (e.g., crunchiness) activates psychosensory, orosensory, and post-ingestive reward mechanisms, which may dysregulate the brain’s reward circuitry for food and contribute to overconsumption and dependency-like patterns[70].

Marketing further exacerbates this issue by capitalizing on adolescent neurodevelopmental vulnerabilities, including limitations of the immature PFC in discerning persuasive intent. Advertisements featuring bright colors, fictional characters, digital platforms, and social media influencers leverage adolescents’ engagement with technology and media—processes central to social identity development-to create positive emotional associations with UPFs and potentially drive overconsumption[69,71,72]. Despite substantial declines in television advertising exposure between 2013 and 2022 (a reduction of 83.8% in food-related advertisements), adolescents still view nearly 1100 unhealthy product advertisements annually, suggesting that voluntary industry self-regulation is insufficient and that broader mandatory policies may be required[73].

A systematic review and meta-analysis of experimental studies manipulating advertising exposure through television or Internet-based platforms and measuring subsequent food intake indicate that children exposed to unhealthy food marketing consume more calories from these products, whereas adults do not. These findings support the need for public health policies aimed at reducing children’s exposure to such advertising[74]. Most evaluations of FOP labeling and taxation policies rely on sales or purchase data rather than direct measures of consumption or body mass index (BMI) outcomes. Reported effect sizes are often small (Cohen’s d < 0.2) and heterogeneous across socioeconomic strata and age groups.

FOP labeling

FOP labeling has been widely implemented as a strategy to reduce UPF consumption and to provide simplified nutritional information that is easily understood by consumers. International public health agencies have endorsed FOP labeling as a key regulatory strategy to reduce the consumption of unhealthy food products. According to the technical guidelines established by the United Nations Children’s Fund and the Pan American Health Organization (PAHO), the objective of FOP labeling systems is to provide clear, visible, and easily interpretable information and to promote healthier food environments by enabling consumers to quickly identify UPFs with high levels of critical nutrients, such as free sugars, saturated and trans fats, sodium, and total energy[75,76].

Different types of FOP labeling are used worldwide in accordance with the public policies implemented by each country or region, and these systems may be either mandatory or voluntary (Figure 3). In the Americas, PAHO uses the Nutrient Profile Model as a standardized tool to determine which products should display warning labels on the front of their packaging. This system is mandatory in most countries and is primarily implemented in Latin America, although in some countries it remains voluntary[77]. The model employs warning octagons and a classification framework that applies to foods and beverages, using maximum permitted thresholds for critical nutrients associated with an increased risk of obesity and noncommunicable diseases (Figure 3)[75]. Despite the growing adoption of FOP labeling across countries in the Americas and other regions, evidence indicates that the effectiveness of these policies varies substantially depending on their design, implementation, enforcement, and regulatory oversight. The implementation of systems based on clear nutritional warning symbols facilitates the provision of accessible and actionable information to consumers regarding the products they purchase. Furthermore, such systems have been shown to encourage product reformulation within the food industry, thereby contributing to reductions in the purchase of foods high in critical nutrients or energy density[78].

Figure 3 Global comparison of front-of-package labeling systems. The figure presents examples of front-of-package labelling approaches implemented across different regions. Mandatory nutrient warning labels have been adopted in countries such as Chile, Mexico, Peru, Argentina, Uruguay, Israel, and Canada. In contrast, voluntary or interpretative systems, including the Health Star Rating (Australia and New Zealand), Nutri-Score (France, Belgium, Germany, Spain, the Netherlands, and Luxembourg), and traffic-light labelling (United Kingdom). Stylized representations are shown for illustrative purposes and to protect copyright.

Conversely, voluntary FOP labeling systems are subject to consumer interpretation and may generate confusion. Examples include the Health Star Rating implemented in Australia and New Zealand, the Nutri-Score voluntarily adopted in several European countries (e.g., France, Belgium, Germany, Spain, and the Netherlands), and the traffic light system used in the United Kingdom (Figure 3). Research has shown that the effects of these systems on consumer behavior are limited or inconsistent[77,79,80]. Their lower effectiveness in influencing consumer decisions is partly attributable to their voluntary application by the food industry, as regulatory frameworks in these countries do not mandate their placement and instead leave implementation optional. In addition, these systems require greater cognitive processing by consumers to interpret the labeling schemes displayed on packaging, some of which present information in percentages or color codes[77,81]. In contrast, the United States does not currently implement a mandatory interpretive FOP warning system. Nutritional information is primarily provided through the standardized Nutrition Facts Panel located on the back of packaging, as required by federal regulation. Although proposals for simplified FOP schemes have been discussed in recent years, no mandatory warning label comparable to those adopted in several Latin American countries or in Canada has been implemented to date[82].

It is important to acknowledge that although FOP warning labels have been shown to enhance awareness and influence the purchasing decisions of adults, who constitute the primary purchasing population, their impact on children and adolescents appears limited[78,81]. In this context, children’s food choices are influenced by multiple factors, including palatability, sensory appeal, emotional associations, brand familiarity, attractive packaging or cartoon characters, visually stimulating advertisements, and food availability within the home environment. These factors often supersede children’s capacity for rational evaluation of nutritional information. This pattern may be related to an imbalance between reward circuitry and executive control networks involved in decision-making during childhood and adolescence, reflecting the immaturity of the PFC[83-85]. Furthermore, parents’ purchasing decisions are frequently influenced by their children’s food preferences, and reciprocal influences may also occur. Parental emotional states, exposure to advertisements and in-store food displays, and related environmental factors can further shape purchasing decisions. Consequently, these interacting influences may attenuate the measurable impact of FOP warning label implementation[69,78].

Moreover, FOP labeling has not been shown to substantially modify the home food environment, where repeated exposure and habitual consumption patterns are established. Although these labeling systems may influence purchasing decisions, they do not directly regulate the availability of UPFs within households or prevent repeated exposure that reinforces individual and family taste preferences and eating habits over time[80,86]. Therefore, although FOP labeling represents an important component of public health policy, it does not address the neurobiological mechanisms underlying excessive UPF consumption driven by heightened reward circuitry vulnerability during neurodevelopment[87,88]. For this reason, Section 5 discusses potential strategies that may help reduce UPF consumption.

Additionally, comparative analyses across regulatory contexts highlight important differences in policy effectiveness. Mandatory FOP warning label systems implemented in Chile and Mexico have been associated with significant reductions in the purchase of sugar-sweetened beverages and high-calorie packaged foods, as well as substantial product reformulation within the food industry[89-91]. In contrast, voluntary or interpretive labeling systems such as Nutri-Score in Europe and the Health Star Rating in Australia have demonstrated more modest and inconsistent effects on consumer behavior[92,93]. Similarly, fiscal measures, including taxes on sugar-sweetened beverages, have been associated with population-level reductions in sales and consumption, although the magnitude of these effects varies and evidence of product substitution has been reported[94,95]. Systematic reviews indicate that labeling and regulatory policies tend to be more effective in adult populations, among whom most studies have been conducted[93]. However, their impact on children’s dietary choices appears more limited, as pediatric food selection is strongly influenced by reward sensitivity, marketing exposure, and environmental factors rather than by cognitive evaluation of nutritional information[74]. This variability underscores that policy effectiveness is highly context-dependent and shaped by regulatory design, enforcement, and population characteristics.

Nutrient-based taxes and restrictions

Fiscal policies, including taxes on sugar-sweetened beverages and energy-dense foods, are designed to regulate consumption by increasing prices and discouraging purchases by distributors and consumers. Studies indicate that the implementation of these taxes can reduce sales of taxed products and, in some cases, decrease total caloric intake at the population level[96,97]. However, nutrient-based taxes primarily influence adult household purchasers; their effects on children and adolescents are largely indirect. Emerging evidence suggests that increases in UPF prices may modestly reduce consumption among youth with disposable income (e.g., pocket money for snacks and beverages)[78,81,87]. Overall, meta-analyses report only small-to-moderate reductions in taxed-product purchases, with even smaller or inconsistent effects on actual caloric intake and BMI z-scores in pediatric populations. In addition, evaluations of taxes on sugar-sweetened beverages have demonstrated product substitution, whereby consumers shift to untaxed alternatives that are similarly energy-dense or equally capable of activating reward circuitry because of their high palatability[98,99]. Likewise, UPFs remain highly accessible and relatively inexpensive, particularly in low-income settings, thereby maintaining high exposure to products containing elevated levels of sugar and saturated fats[100].

From a neurodevelopmental perspective, tax-related measures based on increasing the price of UPFs may have limited capacity to mitigate the hyperreactivity of reward circuitry to foods engineered to maximize sensory appeal and dopaminergic reinforcement[27,37]. It is important to recognize that nutrient-based taxes typically target individual nutrients, such as sugar, rather than the broader category of ultra-processed or potentially addictive foods, thereby allowing many UPFs to maintain a prominent presence within the food environment[100,101]. Consequently, although fiscal measures may contribute to broader strategies for childhood obesity prevention, they remain insufficient to address the neurobiological mechanisms that drive excessive food consumption in pediatric populations.

Elimination of marketing elements targeting children

Regulations restricting marketing to children, including the use of cartoon characters, promotional toys, and child-oriented packaging, have been implemented to reduce the appeal of UPFs to this population. These policies acknowledge the heightened vulnerability of children to marketing influences and the role of branding in shaping early food preferences[102]. However, these regulations remain insufficient because they do not fully account for the neurodevelopmental vulnerability of children and adolescents, whose immature PFC is particularly susceptible to digital marketing and influencer-driven cues[102,103]. Although these measures may reduce explicit advertising directed at children, they do not eliminate exposure to stimuli that activate reward circuitry, as food marketing strategies increasingly rely on digital platforms, social media, influencer promotion, and subtle branding elements that remain largely unregulated. Adolescents, in particular, are highly exposed to digital food marketing, which continues to engage reward-related neural pathways[103].

Therefore, although marketing regulations constitute a necessary component of public health policy, they represent only a partial solution and do not address the underlying neurobiological reinforcement mechanisms associated with addictive-like eating behaviors in children and adolescents.

Nutrition in early life as a fundamental factor in public health policymaking

Nutrition during the early stages of life represents a critical factor that remains insufficiently addressed in current public health policies. This issue warrants attention because neurobiological and behavioral studies have demonstrated that early exposure to sweet flavors influences taste preferences, reward sensitivity, eating behaviors, metabolic regulation, and disease risk later in life, particularly among children under two years of age[104-106]. Furthermore, exposure to sweet flavors begins in infancy, as breast milk reflects maternal dietary patterns and enables infants to become familiar with flavors from an early age[87,107]. However, despite these findings, most public health policies targeting UPF consumption focus primarily on school-age children and adolescents, thereby overlooking early childhood as a critical period for prevention. In addition, regulations rarely address the composition, labeling, or marketing of infant formulas, commercial baby foods, and early complementary feeding products, many of which contain free sugars or promote a preference for sweet taste. Therefore, stricter regulatory measures in this area are warranted[102].

Clearer FOP labeling is also needed for products marketed to children under two years of age, alongside restrictions on marketing practices that normalize or promote sweet taste as desirable or developmentally appropriate. Furthermore, public health strategies should prioritize educational programs for parents that support breastfeeding, responsive feeding practices, and the early introduction of a variety of flavors without added sugars. These approaches have been shown to influence long-term taste preferences and eating behaviors[87,108].

In summary, improving the nutritional environment from birth may represent one of the most effective strategies to reduce reward-driven eating patterns and the long-term impact of childhood obesity. This strategy should include enhanced parental education, the development of self-regulation skills from an early age, and the implementation of behavioral interventions, as discussed in the next section. These early-life nutritional exposures interact with the still-maturing reward and regulatory circuitry described above, potentially amplifying vulnerability to UPFs later in life.

PROPOSED STRATEGIES FOR EFFECTIVE PREVENTION AND INTERVENTION

Parental education and the home food environment

Childhood obesity is associated with poor nutritional patterns influenced by socioeconomic conditions, social determinants, and the family environment. Among these factors, the family environment appears particularly influential, as parental behaviors have been shown to exert a substantial impact on children’s dietary habits. Parents play a central role in shaping their children’s food environment[109]. The home food environment refers to the availability and accessibility of foods within the household[110]. Availability is defined as the presence of specific foods in the home, whereas accessibility refers to parental actions that enable children to obtain foods independently[111]. Having healthy foods readily available at home facilitates the adoption of healthy eating practices, as greater availability and accessibility are associated with increased consumption of these foods[112]. Therefore, the home food environment is shaped by the presence of healthy foods, their accessibility to children, and parental purchasing behaviors based on family preferences, which are subsequently reflected in children’s dietary patterns[113].

Food preferences often reflect familiar dietary exposures from early childhood; therefore, the home environment plays a central role in shaping a healthy relationship with food. Parenting styles influence children’s eating behaviors. Based on this framework, three types of child feeding patterns have been identified: Authoritarian, permissive, and authoritative[114]. Authoritarian feeding emphasizes strict control over dietary intake, including the restriction of unhealthy foods and pressure to consume fruits and vegetables regardless of the child’s preferences. Such practices may increase children’s desire for restricted foods, which are often high in sugar and fat (i.e., UPFs)[115]. Permissive feeding, sometimes referred to as neglectful feeding, occurs when children are allowed to choose what and how much to eat without parental guidance. This approach lacks dietary structure and is associated with increased consumption of nutrient-poor foods[116]. Authoritative feeding represents a balanced approach in which parents provide and encourage healthy food options while allowing the child autonomy in deciding what and how much to consume. This style has been associated with higher intake of fruits and vegetables and lower consumption of UPFs[117]. In practice, authoritative feeding may involve consistent family mealtimes, offering multiple healthy options without coercion, modeling balanced eating behaviors, and applying responsive feeding techniques that respect internal hunger and satiety cues. These strategies are hypothesized to support prefrontal regulatory control over reward-driven eating and to reduce amygdala reactivity to highly palatable food cues. Therefore, the family environment represents a primary context for direct intervention aimed at fostering healthy eating habits. Empirical studies have confirmed that children’s dietary patterns tend to closely resemble those of their parents[118].

Eating habits are defined as the conscious and repetitive patterns through which an individual consumes food, including the types of foods selected, portion sizes, and meal timing in response to social and cultural influences[119]. Family mealtimes are considered a key opportunity to promote healthy eating, as they provide a context in which positive dietary behaviors can be reinforced. Failure to encourage healthy foods from an early age may contribute to selective eating behaviors and increase susceptibility to disordered eating patterns[109].

Parents also transmit their eating behaviors to their children through modeling and daily food-related practices[120]. Similarly, alignment with parental dietary patterns has been shown to directly influence children’s eating behaviors, including the quality, quantity, variety, and frequency of foods consumed[119]. Therefore, strategies aimed at promoting healthy eating in childhood are essential to improve long-term health and quality of life[121].

Dietary patterns are also influenced by parental socioeconomic status. Studies have demonstrated that families with higher socioeconomic status tend to adhere to healthier dietary patterns. Conversely, lower socioeconomic status may limit access to healthy foods and thereby hinder the adoption of healthy eating behaviors[122]. In recent years, the frequency of home-prepared meals has declined, leading to increased consumption of foods high in fat and sugar. This trend may contribute to children’s perception that eating outside the home is normative or desirable; therefore, the promotion of healthy home-cooked meals has been recommended[123].

The home environment and parental nutrition education substantially influence children’s eating behaviors from an early age. Therefore, it is relevant to examine whether a home environment that promotes parental nutrition education and healthy eating behaviors is associated with improved weight regulation in children and whether this association is related to reduced activation of the dopaminergic reward system and lower UPF consumption. Furthermore, it is important to determine whether such effects persist over time, thereby reducing the likelihood of overweight, obesity, or metabolic syndrome later in life. However, achieving these outcomes may be more challenging in socioeconomically disadvantaged settings. Therefore, policymakers should implement measures to improve access to healthy foods for children in these communities.

Development of self-regulation skills from early childhood

As discussed above, the home food environment plays a crucial role in fostering a healthy relationship between children and food from an early age. During early feeding, parents are responsible for determining what and how their children eat, a concept referred to as “food parenting practices”. This framework suggests that children can be taught food-related self-regulation from an early age[124], defined as the individual’s ability to initiate and terminate eating in response to internal hunger and satiety cues[125]. The development of self-regulation is considered a critical process in early childhood, as it lays the foundation for regulatory capacities in adulthood. Therefore, modifications introduced during childhood are important for preventing diet-related diseases later in life[126].

Nutrition constitutes one of the primary domains of parent–child interaction, beginning with breastfeeding and continuing through complementary feeding. The complementary feeding period is particularly important, as children learn to feed themselves and gradually transition toward the family dietary pattern[119]. Conversely, obesity often originates in early childhood and frequently persists into adulthood. For this reason, childhood represents a critical window for intervention in eating behaviors, as children during this developmental stage may be more responsive to behavioral change[127].

Children are born with an inherent capacity to self-regulate food intake; however, this ability may diminish over time as complementary foods are introduced. From that stage onward, children increasingly depend on their parents to provide and structure food choices[128,129]. Beginning at approximately three years of age, the external environment also begins to influence children’s food intake. One relevant factor is the school environment, as some school systems do not restrict access to UPFs[130]. During the preschool years, children may acquire new eating habits more readily through adult modeling, particularly as they spend substantial time within the home environment[131]. Children aged 2-5 years consume at least 75% of their dietary intake at home, underscoring the central role of parents in shaping eating behaviors. For this reason, parents are frequently regarded as key agents of change[132]. From early childhood through early adolescence, parents are primarily responsible for providing food and determining portion sizes and food quality. Larger portion sizes have been associated with weight gain in children. However, these decisions are often based on parental perceptions of appropriate portion size rather than on children’s internal hunger cues. This practice may reduce children’s autonomy in regulating intake, presuppose how much they should consume, and contribute to diminished sensitivity to satiety signals[133]. Satiety and satiation are distinct but related physiological mechanisms involved in appetite regulation and the limitation of food intake[134].

The term “satiety” is often distinguished into two related constructs: intra-meal satiety and post-meal satiety. The former refers to the processes that signal meal termination once immediate physiological needs are met, whereas the latter refers to the suppression of hunger and the reduced motivation to eat between meals[135]. Self-regulation is conceptualized as a multidimensional construct comprising internal processes derived from motor, socioemotional, physiological, behavioral, and motivational functions that facilitate the planning and modulation of behavior at the individual level[126]. Healthy dietary patterns have been associated with better emotional regulation and reduced mealtime pressure. Conversely, emotional dysregulation and maladaptive eating practices are considered risk factors for childhood obesity[136].

In contrast, pressure to eat refers to the extent to which parents encourage or impose specific foods on their children while disregarding their preferences or internal appetite cues[137]. Several studies indicate that healthy family environments that avoid coercive feeding practices are associated with reduced consumption of sugar-sweetened beverages and increased physical activity[138]. Food-related behaviors, such as emotional overeating and heightened enjoyment of food, represent key domains to address in efforts to prevent impaired dietary self-regulation[124]. A child’s ability to self-regulate is influenced by the feeding practices to which they are exposed[139]. Available longitudinal evidence suggests that family-centered interventions initiated in early childhood can produce moderate and sustained improvements in self-regulation, with benefits extending into adolescence when parents consistently apply responsive feeding and structured mealtime practices. These effects are hypothesized to result from repeated positive reinforcement that supports the development of frontostriatal pathways and strengthens the maturing PFC’s capacity to modulate reward circuitry activity[58].

In conclusion, education in food-related self-regulation, a home environment that promotes the availability of healthy foods, and parental nutrition education may help modulate food intake in accordance with internal hunger and satiety cues and the child’s homeostatic needs. Further research is required to determine whether these strategies can modulate reward circuitry, as such modulation could reduce hedonic eating behaviors and the risk of obesity, particularly during the transition from childhood to adolescence and early adulthood, when emotional dysregulation may emerge.

THE ROLE OF PSYCHOLOGICAL THERAPIES IN DISRUPTING DOPAMINERGIC REWARD CIRCUITRY ASSOCIATED WITH UPF OVERCONSUMPTION

As discussed in previous sections, excessive UPF consumption in children and adolescents may be exacerbated by PFC immaturity and hyperactivity of the mesolimbic reward pathway, thereby limiting self-regulatory capacity[13]. Therefore, interventions that promote food-related self-regulation may be essential for disrupting the vicious cycle described in Figure 2.

Psychotherapy represents an important tool for strengthening self-regulation and fostering healthy habits within the home environment[140]. Cognitive behavioral therapy (CBT) and its enhanced form, enhanced CBT (CBT-E), are transdiagnostic approaches that can be adapted to address individual maintenance mechanisms. In contrast, family-based treatment (FBT) places the family at the center of the intervention process[141-143]. Unlike psychoanalytic approaches, which typically involve prolonged exploration of unconscious conflicts and long-term structural change[144], CBT-E and FBT provide structured, present-focused interventions. This orientation aligns with the urgent need to support children and adolescents exposed to addictive-like eating behaviors associated with UPF consumption[145]. Specifically, behavioral strategies such as the normalization of eating patterns and the management of food-related resistance are applied to achieve rapid symptom reduction[146].

FBTs have demonstrated particular efficacy in the management of severe conditions such as adolescent anorexia nervosa. FBTs have been shown to achieve greater weight restoration compared with individual psychotherapies[147,148]. These findings underscore the importance of the family as a central agent of change, particularly during the early phases of treatment, when parents assume responsibility for feeding and externalize the disorder. This approach is especially advantageous when rapid weight restoration is clinically indicated[149]. Psychotherapeutic interventions may provide external regulatory support to protect minors from compulsive eating behaviors associated with UPF consumption[150], while facilitating intake regulation during the maturation of neurobiological self-control mechanisms[145].

THE POTENTIAL FUTURE ROLE OF PHARMACOLOGICAL INTERVENTIONS FOR UPFs OVERCONSUMPTION IN CHILDREN

Addiction to UPFs in children and adolescents is not recognized as a clinical entity in the DSM-5. Therefore, international clinical guidelines do not currently recommend pharmacological interventions that specifically target the neurobiological mechanisms underlying UPF overconsumption, which involve dopaminergic hyperreactivity and reward circuitry dysfunction[142]. Further research is required to determine whether UPF addiction could be incorporated into a distinct diagnostic category in future revisions of the DSM or equivalent classification systems[151]. It is important to distinguish between UPF addiction and the broader construct of food addiction, as not all foods have comparable addictive potential or activate reward circuitry to the same extent as drugs of abuse[150-152]. For this reason, formal recognition of UPF addiction as a diagnostic category may be necessary to facilitate clinical trials and the development of therapeutic guidelines aimed at more targeted pharmacological treatments[59,150].

Future research should first establish a rigorous diagnostic framework for “UPF addiction” in adolescents through prospective multicenter studies combining the YFAS-C, structured clinical interviews, and objective biomarkers such as functional magnetic resonance imaging of striatal reward responses and ecological momentary assessment of cravings. Phase 2/3 randomized, double-blind, placebo-controlled trials should then enroll adolescents aged 14-17 years (with staged extension to 12-13 years after safety is confirmed) who meet strict diagnostic thresholds. These trials should compare a reward-modulating pharmacotherapy (e.g., GLP-1 receptor agonist) plus family-based therapy vs family-based therapy alone over a minimum 12-month follow-up. Primary outcomes include reduction in UPFs consumption, change in BMI z-score, and improvement in compulsive eating scores (YFAS-C). Key safety and neurodevelopmental endpoints must monitor growth velocity, pubertal progression (Tanner staging), emotional regulation, sleep quality, academic performance, and social functioning. Such carefully staged trials are essential before any reward-system-targeting pharmacotherapy can be recommended in pediatric populations. Until such advances are achieved, pharmacological interventions primarily focus on managing comorbid symptoms in adults, such as anxiety and impulsivity, which frequently accompany patterns of compulsive UPF consumption observed in binge-eating disorder and obesity[151]. To mitigate anxiety associated with these patterns, selective serotonin reuptake inhibitors, including fluoxetine and sertraline, have been used. These agents modulate serotonergic neurotransmission to reduce anxiety symptoms and improve emotional regulation in adults[153,154]. Among non-benzodiazepine anxiolytics, buspirone-a partial agonist of the 5-hydroxytryptamine 1A receptor-is primarily prescribed for the treatment of generalized anxiety disorder in adults because of its low potential for dependence[155].

To address impulsivity associated with hedonic intake mediated by opioid pathways, naltrexone blocks μ-opioid receptors to attenuate reward-related pleasure. However, it is typically combined with bupropion, which stimulates proopiomelanocortin neurons in the hypothalamus and promotes the release of α-melanocyte-stimulating hormone. This combination produces a synergistic effect by enhancing satiety signaling and improving inhibitory control in adult patients with obesity[156]. In contrast, topiramate, an anticonvulsant, has been investigated for its capacity to enhance GABA-mediated inhibitory activity and antagonize glutamatergic excitatory transmission. These actions may reduce impulsivity; however, evidence in adolescents with binge-eating disorder indicates only moderate efficacy. Its clinical use remains limited because of adverse cognitive effects and unintended weight loss[150]. Additionally, GLP-1 receptor agonists, such as liraglutide, have been incorporated into obesity management strategies. Liraglutide is approved by the United States Food and Drug Administration and the European Medicines Agency for chronic weight management in adolescents aged 12 years and older with obesity (BMI ≥ 95^th percentile for age and sex), as an adjunct to a reduced-calorie diet and increased physical activity. Although emerging evidence suggests that GLP-1 receptor agonists may attenuate reward-driven eating behaviors, these agents are not indicated or approved for the treatment of food addiction, compulsive UPF overconsumption, or binge-eating disorder[157]. Current evidence for GLP-1 receptor agonists in eating disorders is derived largely from adult trials; pediatric data are limited to weight-management indications, and their effects on developing reward circuitry remain uncertain.

According to current clinical guidelines, pharmacological intervention is recommended only as an adjunct to lifestyle management. It is considered after a rigorous evaluation of the risk–benefit ratio in relation to the growth and neurodevelopment of children and adolescents. In this context, the limited evidence extrapolated from adult populations underscores the urgent need for controlled clinical trials to establish the efficacy and long-term safety of pharmacological interventions in pediatric populations[158]. Consequently, future research should further investigate reward circuitry to facilitate the development of targeted pharmacological strategies aimed at reducing addictive-like eating behaviors. However, given evolving diagnostic criteria, ongoing debates regarding “food addiction” as a clinical entity, the unique neurodevelopmental vulnerabilities of children and adolescents, and the paucity of long-term safety and efficacy data, such interventions should be regarded as a priority area for rigorous clinical research rather than as current therapeutic recommendations. Any future implementation would require carefully designed pediatric trials with comprehensive neurodevelopmental monitoring.

CONCLUSION

The childhood obesity epidemic may be associated with excessive UPF consumption, as these products-due to their engineered hyper-palatability-may promote compulsive eating behaviors resembling addiction through activation of dopaminergic reward circuitry. This vulnerability may be amplified in pediatric populations by PFC immaturity and hyperreactivity of reward circuitry, potentially resulting in impaired self-regulation, obesity, and, in the medium to long term, the development of T2D (Figure 4). In an effort to reduce UPF consumption, regulatory measures such as FOP labeling, nutrient-based product taxation, and restrictions on child-targeted marketing have been implemented. However, these measures appear to be limited in effectiveness because, similar to traditional dietary interventions, they do not address the neurobiological mechanisms underlying excessive UPF consumption (Figure 4). Additional factors-including unclear labeling in certain contexts, voluntary implementation in some countries, and lack of regulatory harmonization-further diminish their impact. Moreover, taxation of UPFs does not directly influence children’s purchasing behavior, as food purchasing decisions are typically made by parents. In this context, parents play a pivotal role in fostering their children’s self-regulation skills. This role includes the strategic management of food availability within the home and the cultivation of positive eating habits. Similarly, psychotherapeutic interventions aimed at preventing addictive-like tendencies associated with excessive UPF consumption may complement parental education efforts. The recognition of UPF addiction as a clinical entity remains speculative. Pharmacological management in severe pediatric cases would require rigorous clinical trials assessing safety and efficacy, with long-term neurodevelopmental monitoring. Current evidence does not support the use of these agents in children. Therefore, impulsive UPF consumption may be more effectively addressed through a comprehensive approach centered on parents, including improvement of the home food environment and provision of nutrition education from early childhood, in conjunction with family-based therapy (Figure 4). Well-designed randomized controlled trials in adolescents are essential to evaluate the safety and efficacy of reward-modulating agents before any pharmacological strategy can be recommended for pediatric populations.

Figure 4 Proposed multitargeted intervention to prevent ultra-processed foods overconsumption in children and adolescents. The upper panel illustrates the current limitations of public health policies [taxes on ultra-processed foods (UPFs), front-of-package labeling, and restrictions on child-targeted marketing]. These policies primarily target the obesogenic environment but fail to address the core neurodevelopmental vulnerabilities: A hyper-reactive reward circuit combined with an immature prefrontal cortex (PFC) that provides limited impulse control. This imbalance leads to excessive dopamine release triggered by UPFs consumption, promoting compulsive and addictive-like eating behaviors, which in turn contribute to obesity and metabolic diseases. Traditional dietary interventions are shown as having limited impact because they do not target the underlying neurobiological mechanisms. The lower panel proposes a comprehensive multi-targeted intervention model. On the left side, it emphasizes the recognition of UPFs addiction as a clinical condition (aligned with Diagnostic and Statistical Manual of Mental Disorders, fifth edition criteria for binge-eating disorder and related disorders) as a necessary prerequisite to enable rigorous research on pharmacological therapies already used in adults for weight management. These include selective serotonin reuptake inhibitors, buspirone, bupropion combined with naltrexone (opioid pathway modulation), and GLP-1 agonists such as liraglutide. On the right side, the model highlights family-centered strategies as the central and immediately actionable pillar: (1) Parental nutrition education; (2) Family-based treatment; and (3) Modification of the home food environment to increase the availability and accessibility of healthy foods. These interventions aim to strengthen children’s self-regulation skills, reduce exposure to UPFs cues, and support the maturing PFC in exerting greater inhibitory control over reward-driven eating. Arrows indicate the proposed transition from current policy limitations toward an integrated approach that combines neurobehavioral, family-based, and potential future pharmacological strategies. UPF: Ultra-processed foods; DSM-5: Diagnostic and Statistical Manual of Mental Disorders, fifth edition.