Emerging Therapeutic Strategies for Infantile Obesity: A Narrative Review

1. Introduction

Childhood obesity is a major clinical problem diffused worldwide [1]. When obesity is not consequent to endocrinological, monogenic or syndromic disorders it can be considered ‘essential’ obesity, consequent to a multifactorial pathogenesis. This is a chronic, relapsing, and multifactorial disease arising from interactions among biological susceptibility, eating behavior, environmental exposures, and socioeconomic conditions. In children and adolescents, body mass index (BMI) must be interpreted by age and sex. For individuals aged 5–19 years, the World Health Organization (WHO) defines overweight as BMI-for-age greater than one standard deviation above the reference median and obesity as greater than two standard deviations; comparisons across studies must nevertheless account for differences between WHO and International Obesity Task Force classification systems [1,2].

The global burden has increased sharply. In 2022, more than 390 million people aged 5–19 years were living with overweight, including approximately 160 million with obesity, and the prevalence of overweight in this age group had risen from about 8% in 1990 to 20% in 2022 [1,3]. In the sixth round of the WHO European Childhood Obesity Surveillance Initiative, 25% of children aged 7–9 years were living with overweight, including 11% with obesity [4]. Italian surveillance similarly indicates that approximately three in ten children aged 8–9 years have excess weight, with higher prevalence in southern regions [5]. Socioeconomic inequalities are marked: analysis of 53,275 Italian children showed less favorable dietary and activity patterns and higher obesity prevalence among children from families with lower parental education [6].

Pediatric obesity is associated with hypertension, insulin resistance, type 2 diabetes, dyslipidemia, metabolic dysfunction-associated steatosis liver disease, obstructive sleep apnea, and other early or adult complications. It also frequently persists into adulthood and predicts later cardiometabolic morbidity and premature cardiovascular mortality [7,8,9,10]. Its burden is also psychological and social: weight stigma, bullying, body dissatisfaction, anxiety or depressive symptoms, impaired quality of life, and disordered eating may occur, although these outcomes are heterogeneous and should not be assumed in every child [11,12,13]. Neurodevelopmental comorbidity is relevant in selected patients. ADHD is associated with a modest increase in pediatric overweight and obesity but overlapping reward-related behavior and ADHD-specific cognitive-control difficulties appear partly distinct [14,15,16].

According to its complex pathogenesis and clinical expression, treatment cannot be reduced to dietary prescription. Contemporary care combines nutrition, physical activity, behavioral strategies, psychological support, and family involvement, while accounting for treatment accessibility and social context [10,17]. Recently the therapeutic landscape has also expanded. While intensive nutritional, behavioral and family-based interventions remain foundational, some new drugs such as liraglutide, semaglutide, and other anti-obesity medications can produce rapid and clinically meaningful BMI reductions in selected young people. Their long-term safety, durability after discontinuation, accessibility, and integration with psychological and family care remain incompletely defined [18,19,20].

2. Materials and Methods

The aim of the present review is to discuss the most recent interplay among psychological, family-based, and pharmacological approaches to pediatric obesity, with focused consideration on treatment engagement, eating psychopathology, and some limited evidence concerning the relationship between obesity, ADHD, and stimulant-associated weight trajectories.

This narrative review was supported by a structured literature search designed to identify studies directly relevant to the multidisciplinary management of pediatric obesity, with particular attention to psychological and family-related factors, eating psychopathology, neurodevelopmental comorbidities, treatment engagement, and pharmacological approaches. Literature was identified using PubMed/MEDLINE, Scopus, and Web of Science, supplemented by backward and forward citation tracking of key publications. The search primarily covered studies published from 2010 to August 2026, with particular emphasis on recent evidence from 2015–2026, while retaining earlier landmark studies when necessary to establish relevant epidemiological, clinical, neurobehavioral, or therapeutic findings.

Search terms were used in different combinations and included “pediatric obesity”, “childhood obesity”, “adolescent obesity”, “overweight”, “multidisciplinary treatment”, “lifestyle intervention”, “behavioral intervention”, “family-based treatment”, “psychological intervention”, “cognitive behavioral therapy”, “motivational interviewing”, “emotional regulation”, “treatment adherence”, “attrition”, “socioeconomic factors”, “telehealth”, “depression”, “anxiety”, “weight stigma”, “body dissatisfaction”, “eating disorders”, “binge eating”, “loss-of-control eating”, “ADHD”, “attention-deficit/hyperactivity disorder”, “executive function”, “impulsivity”, “inhibitory control”, “delay discounting”, “reward processing”, “neuroimaging”, “stimulant treatment”, “methylphenidate”, “lisdexamfetamine”, “anti-obesity medication”, “GLP-1 receptor agonist”, “liraglutide”, “semaglutide”, “orlistat”, and “phentermine/topiramate”. Additional targeted searches were conducted when specific clinical, neurobehavioral, treatment-related, or pharmacological questions emerged during manuscript development.

Priority was given to peer-reviewed studies directly examining pediatric obesity and its treatment, including randomized controlled trials, prospective and retrospective cohort studies, large observational and real-world studies, and clinically relevant cross-sectional investigations. Systematic reviews, meta-analyses, and international clinical guidelines were used to characterize the broader evidence base, identify relevant primary studies, and provide context for areas supported by a large or heterogeneous literature. Official reports from recognized public-health institutions, including the World Health Organization and the Italian National Institute of Health, were also considered for epidemiological and surveillance data.

Studies involving children and adolescents younger than 18 years were prioritized. Studies including both pediatric and adult participants were retained when pediatric findings were reported separately or when they provided information directly relevant to the aims of the review. Adult-only studies were generally excluded from the main evidence synthesis; however, selected adult studies were retained solely as contextual evidence when controlled pediatric data were unavailable, including studies on binge-eating disorder treated with lisdexamfetamine, post-treatment weight trajectories after semaglutide withdrawal, and family engagement or treatment resistance in eating disorders. Findings derived from adult populations were interpreted as indirect or hypothesis-generating evidence and were not considered evidence of efficacy or safety in children and adolescents. The limited pediatric observational evidence on stimulant treatment and loss-of-control eating was considered separately and was not treated as evidence supporting routine clinical use.

Studies focusing primarily on monogenic or syndromic obesity were not included unless they provided information directly applicable to the broader clinical questions addressed in the review. Duplicate publications, conference abstracts, non-peer-reviewed sources, and studies without a direct connection to pediatric obesity, its psychological or neurodevelopmental correlates, treatment engagement, or therapeutic management were excluded. Narrative reviews were used mainly to identify relevant concepts and primary studies rather than as the principal source for quantitative estimates whenever original evidence was available.

3. Results

3.1. Multicomponent Lifestyle and Behavioral Interventions

Intensive health behavior and lifestyle treatment combines nutritional counseling, physical activity, reduced sedentary behavior, and behavioral techniques, usually with family participation. The 2023 American Academy of Pediatrics guideline recommends family-based, multicomponent treatment and identifies at least 26 contact hours over 3–12 months as the most effective available intensity; programs at this level were associated with clinically significant improvements in BMI, systolic and diastolic blood pressure, fasting glucose, and insulin [10,21]. In the technical evidence review supporting the guideline, Skinner and coworkers included 215 intervention studies, but psychosocial outcomes were reported in only about 20% of the studies and mental-health outcomes in 5%, confirming that the evidence supporting clinical guidelines remains predominantly weight-centered [21].

Greater intensity of behavioral interventions appears to improve anthropometric outcomes [22]. Effective programs commonly use self-monitoring, goal setting, problem solving, environmental restructuring, modeling, and relapse-prevention strategies. A systematic review found that management interventions used a mean of 7.5 behavior-change techniques, but specific psychological components, such as emotion-regulation training and motivational interviewing, were rarely included. Moreover, intervention effectiveness was not explained simply by the total number of behavior-change techniques used, suggesting that their selection, implementation, and adaptation to the child and family may be more important than their quantity alone [23].

3.2. Psychological and Family-Based Interventions

Evidence emerging from a wide randomized clinical study supports family-based behavioral treatment. In 452 children aged 6–12 years, a primary-care intervention targeting eating, physical activity, and parenting practices produced a greater reduction in percentage above median BMI than usual care at 24 months (between-group difference −6.21 percentage points, 95% CI −10.14 to −2.29); benefits also extended to participating family members with excess weight [24]. In the smaller ENTREN/ENTREN-F three branches trial both the intervention protocols incorporated nutritional approach, support to physical activity, support in emotional regulation, attention paid to body image, and to social functioning of participants. Adding parallel sessions for parents was associated with better adherence, reduction in the BMI z-score, reduction of child anxiety, and family adaptability, although the sample of 70 children limits definitive conclusions [25].

The pragmatic TEAM UP trial extended these findings to 730 children and adolescents across 41 primary-care practices. At 12 months, enhanced standard care plus family-based behavioral treatment reduced percent median BMI more than enhanced standard care alone (between-group difference −3.8 units, 95% CI −6.20 to −1.34; p = 0.002). The study included substantial socioeconomic diversity, with 47% of participants insured by Medicaid and 22% reporting household food insecurity, supporting the feasibility of family-based treatment in routine primary care [26].

3.3. Treatment Engagement and Feasibility

Participation in treatment protocols for child obesity is limited by time availability among family members (parents’ work and childcare, and children’s school commitments), transportation, financial costs, and the complexity of treatment information. In a systematic review of 26 studies, perceived benefit, professional recommendation, financial incentives, and practical or social support were the most frequent facilitators [27]. In the ENTREN/ENTREN-F trial, mean attendance was 72.4% in ENTREN-F and 68.2% in ENTREN, versus 54.9% in the brief control condition (overall p = 0.001); the control group attended significantly less than both ENTREN (p = 0.017) and ENTREN-F (p = 0.001), while the two multidisciplinary programs did not differ significantly [28]. Lower attendance was also associated with lower maternal education, higher maternal depressive symptoms, more maternal critical comments toward the child, and greater child weight severity; logistical barriers accounted for 47.9% of reported attrition reasons [28].

All the abovementioned barriers intersect with socioeconomic inequalities in obesity risk [6]. Nevertheless, since logistical difficulties were the most frequently reported barriers, remote or hybrid care may reduce treatment burden, although evidence remains preliminary and engagement may still be limited by less readily recognized psychological factors. In an Italian telehealth program, 117 of 156 eligible patients (75.0%) participated during the COVID-19 lockdown; 75 participants (64.1%) returned for post-lockdown assessment, compared with only 7 of 39 nonparticipants (17.9%). This marked differential follow-up and the very small comparison group limit conclusions to feasibility rather than comparative efficacy [29].

3.4. Psychopathology and Disordered Eating

Psychopathological comorbidity and eating disorders (BED in particular) are clinically sound but display heterogeneous manifestation, often in comorbidity with each other. In a treatment-seeking sample of 170 Spanish children aged 8–12 years with overweight or obesity, all participants underwent a standardized diagnostic interview and questionnaires assessing anxiety, depression, and disordered eating. As a result, 57.1% of the participants met criteria for at least one psychiatric disorder, and 33.5% reported loss-of-control eating [30]. Moreover, as recommended by authors, children without a categorical diagnosis of a psychiatric disorder could still have had subthreshold symptoms or minor neurodevelopmental disorders, hence these estimates cannot be considered exhaustive of the psychopathological problems associated with obesity and generalized to community populations. In particular, symptoms such as emotional eating, eating in the absence of hunger, loss-of-control eating, binge-eating, restrictive dieting, body dissatisfaction, and weight-related stigma may often occur even if they are not included in a specific DSM categorization, and thus require targeted assessment and tailored treatment [12].

Prospective evidence suggests possible bidirectional relationships between obesity and eating-disorder symptoms, whereas findings for depression vary by age and sex and evidence for anxiety remains insufficient [13]. Psychological outcomes are generally assessed longitudinally with structured interviews or validated measures, but instruments and thresholds vary, and underthreshold symptoms may still interfere with eating behavior and obesity treatment. The absence of a categorical diagnosis should therefore not be equated with absence of clinically relevant symptoms [13]. Concern that obesity treatment might exacerbate eating psychopathology arises primarily from observational associations between self-reported dieting outside professionally supervised treatment and subsequent disordered-eating behaviors, rather than from evidence that professionally supervised dietary treatment causes eating disorders [31]. Jebeile et al. synthesized 36 pediatric obesity-treatment studies involving 2,589 participants. All interventions combined a dietary component with behavior-modification strategies; some also addressed eating-disorder-related content, eating behaviors, or body image, and a psychologist, counsellor, or therapist was involved in 17 studies. At post-treatment, binge eating (SMD −0.588, p < 0.001), bulimic symptoms (SMD −0.326, p < 0.001), emotional eating (SMD −0.149, p = 0.008), and drive for thinness (SMD −0.167, p = 0.005) decreased; overall eating-disorder risk was also reduced at follow-up (SMD −0.313, p = 0.012). Moderator analyses found no significant effect of psychologist involvement on change in eating-disorder risk, so the observed improvement cannot be attributed specifically to psychotherapy. Overall, structured and professionally supervised obesity treatment with a dietary component did not, on average, worsen eating psychopathology and improved several related symptoms. Continued monitoring remains appropriate because eating-disorder prevalence was reported in only five studies and participants who withdrew from treatment were poorly represented [31].

3.5. ADHD and Related Neurobehavioral Considerations

Among psychopathological disorders relevant for childhood obesity a specific attention should be devoted to the Attention Deficit Disorder (ADHD). ADHD is associated with a modest increase in pediatric overweight and obesity, but the relationship should not be overstated [14,15]. Small specialist-clinic studies suggest that previously unrecognized neurodevelopmental disorders may be concentrated among children seeking specialist obesity treatment and may be relevant for its pathogenesis, but referral and selection effects prevent extrapolation to all children with obesity [32]. Therefore, ADHD screening is reasonable in the child obese population when attentional or organizational difficulties, school impairment, impulsivity, or repeated failure to follow structured recommendations persist despite adequate support; a positive screen must be followed by a full diagnostic assessment.

As it concerns psychopathology, current evidence supports partly shared but distinguishable pathogenic mechanisms among obesity and ADHD. Reward sensitivity and reward-related decision-making may overlap in ADHD and overweight/obesity, whereas impaired cognitive control appears more specifically associated with ADHD [16]. Dopaminergic and noradrenergic signaling provides a plausible neurobiological link, but current behavioral and neuroimaging findings do not support a single dopamine-deficiency explanation or justify describing ADHD and obesity as one “reward deficiency syndrome” [33]. Clinically, shorter goals, immediate non-food reinforcement, reminders, predictable routines, and parental scaffolding are plausible adaptations for executive-function difficulties, although they have not been specifically validated in randomized obesity trials involving children with ADHD.

As concerns treatment even though the use of amphetaminic stimulants could be suggestive for the treatment of child obesity, some caveats need to be posed. Stimulants are treatments for ADHD, not anti-obesity medications. Observational and meta-analytic data suggest small early reductions in weight or BMI during stimulant treatment, with a need for individualized growth and nutritional monitoring; longitudinal data also raise the possibility of later BMI rebound [34,35,36]. Their possible effect on disordered eating is clinically relevant but remains preliminary. In a retrospective chart review of 25 adolescents aged 12–19 years with BED treated with lisdexamfetamine, 15 reported some improvement in BED symptoms, but BMI percentile did not decrease significantly [37]. In a prospective uncontrolled study of 10 children aged 8–13 years with ADHD and loss-of-control eating who started methylphenidate or lisdexamfetamine, mean loss-of-control episodes decreased from 10.3 to 2.1 over three months, with improvement reported in nine participants [38]. In adult treatment responders, continued lisdexamfetamine reduced six-month BED relapse compared with placebo (3.7% vs. 32.1%), but this outcome concerned binge-eating relapse rather than maintenance of weight loss; adult randomized and meta-analytic findings cannot establish pediatric efficacy or safety [39,40]. These signals justify controlled pediatric trials but not the systematic use of stimulants as weight-loss treatment. Moreover such trials must separate effects on ADHD symptoms, loss-of-control eating, weight, growth, cardiovascular safety, and misuse risk.

3.6. Pharmacological Treatment

Pharmacotherapy for obesity is increasingly used as an adjunct to behavioral treatment, especially in adolescents with more severe obesity unresponsive to dietary and behavioral treatment. Torbahn and coworkers summarized an updated Cochrane systematic review evaluating the benefits and harms of anti-obesity medications in children and adolescents. The systematic review included 35 randomized trials involving 4,331 participants; 25 trials involving 3,088 participants contributed to the BMI meta-analysis. Compared with the same behavioral intervention with or without placebo, pharmacotherapy produced an overall BMI reduction of 1.71 kg/m² (95% CI, −2.27 to −1.14). Drug-specific subgroup estimates were −5.88 kg/m² for semaglutide, −4.57 kg/m² for phentermine/topiramate, −1.70 kg/m² for sibutramine, −1.58 kg/m² for liraglutide, −1.27 kg/m² for metformin, −1.00 kg/m² for exenatide, and −0.79 kg/m² for orlistat. However, these estimates were derived from separate and heterogeneous trials rather than head-to-head comparisons; semaglutide and phentermine/topiramate were each represented by only one trial. Therefore, the larger numerical reductions observed with these two agents should not be interpreted as a formal comparative ranking [41,42]. Treatment effects varied substantially across agents, and evidence regarding long-term safety, weight regain, use in younger children, and underrepresented populations remained limited. Older pharmacological approaches produced comparatively modest effects in individual trials. Six months of metformin reduced BMI by 1.09 kg/m² compared with placebo in children with obesity and insulin resistance [43]. In a one-year randomized trial involving 539 adolescents, orlistat reduced BMI by 0.55 kg/m², whereas BMI increased by 0.31 kg/m² with placebo (p = 0.001). A BMI reduction of at least 5% was achieved by 26.5% of participants receiving orlistat versus 15.7% receiving placebo, while reductions of at least 10% occurred in 13.3% versus 4.5%, respectively. Gastrointestinal adverse events were generally mild to moderate but occurred more frequently with orlistat (9%–50% versus 1%–13%) [44]. Among newer pharmacological options, placebo-controlled trials reported larger percentage reductions in BMI, although differences in study design preclude direct comparisons between agents. In adolescents, liraglutide produced a placebo-adjusted difference in the percentage change in BMI of −4.64 percentage points at 56 weeks, whereas once-weekly semaglutide produced a difference of −16.7 percentage points at 68 weeks [18,19]. Phentermine/topiramate produced placebo-adjusted differences of −8.11 percentage points with the mid dose (7.5/46 mg) and −10.44 percentage points with the top dose (15/92 mg) at 56 weeks [45]. Gastrointestinal adverse events were frequent with both GLP-1 receptor agonists. With liraglutide, they occurred in 64.8% of participants versus 36.5% with placebo and mainly included nausea (42.4% vs. 14.3%), vomiting (34.4% vs. 4.0%), and diarrhea (22.4% vs. 14.3%). With semaglutide, gastrointestinal events occurred in 62% versus 42%, including nausea (42% vs. 18%), vomiting (36% vs. 10%), diarrhea (22% vs. 19%), and abdominal pain (15% vs. 6%). These events were generally mild or moderate and occurred mainly during or shortly after dose escalation. Cholelithiasis was reported in 4% of participants receiving semaglutide and in none receiving placebo [18,19]. Evidence in younger children is emerging, in a trial involving 82 children aged 6 to <12 years, liraglutide produced a 7.4-percentage-point greater reduction in BMI than placebo at 56 weeks [46].

Despite the promising evidence regarding newer anti-obesity medications, important uncertainties remain, particularly concerning the maintenance of weight reduction after treatment discontinuation. Direct pediatric evidence is available from randomized trials of liraglutide. In the trial involving 251 adolescents, liraglutide produced a placebo-adjusted reduction in BMI of 4.64 percentage points after 56 weeks of treatment. However, during the subsequent 26-week off-treatment period, BMI standard-deviation scores increased significantly more among participants previously receiving liraglutide than among those previously receiving placebo (estimated difference, 0.15; 95% CI, 0.07–0.23), indicating partial loss of the treatment effect after discontinuation [18]. A similar pattern was observed in the trial involving 82 children aged 6 to <12 years. At week 56, mean BMI had decreased by 5.8% with liraglutide and increased by 1.6% with placebo, corresponding to a treatment difference of −7.4 percentage points. During the following 26 weeks without treatment, BMI and body weight increased in both groups. Nevertheless, at week 82, mean BMI remained 0.8% below baseline among children previously treated with liraglutide, whereas it was 6.7% above baseline in the placebo group, suggesting that weight regain occurred but that part of the treatment benefit persisted [46].

These controlled findings are supported by real-world pediatric data. A large retrospective study conducted in Israel examined 307,208 children and adolescents aged 10–18 years with overweight or obesity, of whom only 2,236 (0.7%) were prescribed metformin, liraglutide, or orlistat [47]. Among the 1,717 participants with at least two medication dispensations, metformin—used off-label for obesity—was the most frequently prescribed medication (73.8%), followed by liraglutide (24.5%) and orlistat (1.7%). Median treatment duration was approximately 1.5–1.7 years for metformin and approximately 0.6 years for liraglutide and orlistat. Semaglutide was not included because data on its pediatric use were not available during the study period. Overall, 55.1% of treated participants achieved a maximal reduction in BMI z-score greater than 0.2 SD, with no significant differences among metformin, liraglutide, and orlistat (53.9%, 57.3%, and 58.3%, respectively; p = 0.588). Treatment was also associated with reductions in blood glucose, HbA1c, triglycerides, and total cholesterol and with an increase in HDL cholesterol. After treatment discontinuation, BMI z-scores and cardiometabolic parameters partially regressed toward pretreatment values, although they remained significantly improved compared with baseline. These observational findings confirm that post-treatment weight regain can occur in routine pediatric practice while also suggesting that some anthropometric and metabolic benefits may persist. However, they do not establish long-term durability and cannot be directly extrapolated to newer agents, particularly semaglutide [47].

The proportion of adolescents with obesity prescribed an FDA-approved obesity medication increased from 0.1% in 2020 to 0.5% in 2023, corresponding to an adjusted increase of approximately 302% [48]. The medications considered were orlistat, phentermine, phentermine/topiramate, setmelanotide, high-dose liraglutide, and high-dose semaglutide, rather than GLP-1 receptor agonists alone. In 2023, semaglutide was the most frequently prescribed medication, accounting for 57.1% of treated adolescents, followed by phentermine or phentermine/topiramate (37.7%) and liraglutide (11.9%). Despite the relative increase, treatment reached only 0.5% of adolescents with obesity. Moreover, Black adolescents were 39% less likely than White adolescents to receive a prescription, even though severe obesity was more prevalent among them. High out-of-pocket costs, insurance restrictions, medication shortages, and differences in prescribing practices may contribute to this limited and unequal access [48]. Overall, available trials demonstrate increasingly large short-term reductions in BMI, but evidence remains limited regarding weight maintenance after treatment withdrawal, long-term safety across growth and puberty, equitable access, and the integration of pharmacotherapy with sustained psychological and family-based care [20,41].

4. Discussion

Treatment of child obesity is still a challenging issue for public health and welfare. New therapeutic instruments are now available, with moderate-to-good evidence of efficacy [10,18,19,20,21,24,25,26,41,42,43,44,45,46,47,48]. Nevertheless, concerns persist regarding the short- and long-term effectiveness of treatment protocols, particularly pharmacological treatments, as well as logistical, economic, and psychological barriers [20,25,27,28,29,41,47,48]. Intensive lifestyle and behavioral interventions remain foundational, but their effectiveness is shaped by psychological functioning, eating behavior, family organization, socioeconomic resources, neurodevelopmental characteristics, and treatment accessibility [21,22,23,24,25,26,27,28,29,30]. Pharmacotherapy has produced substantially larger average BMI reductions, yet it does not replace the need for long-term, multidisciplinary care [10,20,41,42].

Along with the persisting needs for improvement of therapeutic effectiveness, treatment availability and compliance, and for the multidisciplinary integration of available treatments, some general issues emerge from the current review.

4.1. Beyond a Predominantly Weight-Centered Model

The first is a methodological issue: the available literature remains disproportionately focused on anthropometric outcomes. In the evidence review supporting the AAP guideline, psychosocial and mental-health outcomes were reported far less often than weight-related outcomes, despite the behavioral framing of most interventions [21]. BMI change is clinically important, but it does not capture body image, emotional regulation, eating psychopathology, family functioning, social participation, or quality of life. These domains are critical for the evolutionary age and may be influential on the development of the child independently from the physical consequences of being overweight. Conversely, improvement in these domains may be meaningful even when short-term BMI change is modest. A child whose BMI decreases while loss-of-control eating, depression, or major family and treatment burdens remain unchanged may have achieved an anthropometric response without a complete or durable therapeutic response.

Emotional symptoms may not be spontaneously recognized or reported by children and can be expressed through developmental changes in irritability, withdrawal, sleep, interests, school functioning, or eating behavior. Assessment should therefore integrate the child’s account, caregiver observations, and clinical evaluation, with specialist assessment when clinically indicated [10,17]. This broader framework should not be interpreted as an indication for psychotherapy in every child with obesity. Anxiety, depressive symptoms, body dissatisfaction, and disordered eating are more frequent in some clinical subgroups but are neither universal nor necessarily caused directly by adiposity [13,17]. The available meta-analytic evidence suggests that loss-of-control eating is particularly relevant because it describes the child’s relationship with food more directly than BMI and may indicate a need to address emotional regulation or eating psychopathology. The findings of Jebeile and coworkers challenge the assumption that professionally supervised dietary treatment necessarily worsens eating pathology: on average, several disordered-eating symptoms improved during and after treatment [31]. This suggests that addressing impulsive eating and encouraging the management of emotions on a different ground with respect to food intake may be effective also with a nutritional approach. Psychopathological screening and longitudinal psychological monitoring should therefore accompany treatment, without allowing a generalized fear of triggering an eating disorder to prevent access to appropriate obesity care.

4.2. Family Context and Treatment Feasibility

Family-based trials show that caregivers can support changes in meal routines, food availability, reinforcement, physical activity, and environmental cues, with benefits demonstrated in both specialist and primary-care settings [24,25,26]. Although evidence from anorexia nervosa is not direct evidence for pediatric obesity, it reinforces the broader principle that family involvement should be framed as a therapeutic resource rather than as attribution of causal responsibility for the child’s weight [49].

Engagement depends partly on whether families can attend the scheduled contacts and translate recommendations into everyday routines. Time, transportation, work schedules, childcare, cost, parental distress, and socioeconomic disadvantage can reduce attendance and the treatment dose received [27,28]. Repeated non-attendance should therefore be treated as clinical information about a possible mismatch between treatment demands and family resources, rather than as automatic evidence of poor motivation. Evidence from adults with severe and enduring anorexia nervosa suggests that treatment resistance may require psychologically informed and individually adapted goals; whether this approach improves adherence in pediatric obesity remains untested [50]. Flexible scheduling, simplified plans, delivery through primary care, and remote or hybrid follow-up may improve access. Telehealth data support feasibility, but current evidence is insufficient to regard remote treatment as universally equivalent to face-to-face multidisciplinary care [29].

4.3. Pharmacotherapy Within Multidisciplinary Care

Across separate placebo-controlled trials, semaglutide, liraglutide, and phentermine/topiramate produced larger average BMI reductions than older agents, although the absence of head-to-head comparisons precludes a formal ranking [18,19,41,42,45]. Nevertheless, greater efficacy should not create a new therapeutic reductionism. Medication can alter appetite, satiation, and energy intake but does not directly resolve weight stigma, family conflict, depression, treatment barriers, or disordered eating.

The chronic nature of obesity is particularly evident after treatment cessation. In the adolescent liraglutide trial, the 26-week off-treatment period was associated with a greater increase in BMI standard-deviation score among participants previously receiving liraglutide than among those previously receiving placebo (estimated difference, 0.15; 95% CI, 0.07–0.23) [18]. This does not contradict the BMI reduction observed during active treatment; rather, it indicates partial loss of the treatment effect after withdrawal. The same pattern emerged among children aged 6 to <12 years: BMI and body weight increased after liraglutide discontinuation, although mean BMI at week 82 remained below baseline in the former liraglutide group [46]. Real-world Israeli data likewise showed an increase in BMI z-scores and partial regression of cardiometabolic improvements after medication cessation, although values remained better than pretreatment levels [47]. Contextual adult evidence from the STEP 1 extension strengthens this concern but cannot be directly extrapolated to pediatric patients: one year after semaglutide 2.4 mg and lifestyle intervention were withdrawn, participants had regained 11.6 percentage points, approximately two-thirds of the 17.3% mean weight loss achieved during treatment, and most cardiometabolic improvements had moved toward baseline [51]. Collectively, these findings are consistent with obesity as a chronic, relapsing disease and indicate that durability after withdrawal should be considered part of efficacy rather than a secondary concern [10,20,51]. However, medication may suppress appetite without modifying emotional distress, loss-of-control eating, family difficulties, or neurodevelopmental barriers that contribute to obesity maintenance; these unaddressed factors could limit treatment durability. Longer follow-up is needed to define safety across growth and puberty, treatment duration, discontinuation strategies, nutritional adequacy, body composition, and psychological effects.

Access to anti-obesity medications is another limitation: in U.S. real-world data, prescribing remained uncommon and socially patterned. Possible barriers include high out-of-pocket costs, insurance restrictions, medication shortages, and differences in prescribing practices; the study considered all FDA-approved obesity medications, not GLP-1 receptor agonists alone [48].

A short medication course should therefore not be presented as a permanent solution.

4.4. Clinical Implications, Limitations, and Future Directions

The overall assessment of child obesity should extend beyond BMI and metabolic complications to include eating patterns, loss-of-control eating, emotional symptoms, body dissatisfaction, weight-related victimization, family functioning, and practical barriers to treatment [10,12,13,17,21,27,30,31]. Because children may not spontaneously identify or report internalizing symptoms, assessment should be multi-informant and followed by specialist evaluation when indicated [10,13,17]. Neurodevelopmental evaluation should be targeted rather than universal and should never infer ADHD from obesity, overeating, or poor adherence alone [14,15,16,32,33]. When ADHD is confirmed and stimulant treatment is clinically indicated, appetite, nutritional intake, height, weight, BMI trajectory, and blood pressure should be monitored longitudinally [34,35,36].

The present review has limitations. Its narrative design does not provide the reproducibility or pooled estimates of a systematic review, and the included literature is heterogeneous in age, obesity definition, setting, intervention intensity, follow-up, and outcome selection. Evidence on psychological and neurodevelopmental phenotypes is often cross-sectional or observational, whereas pharmacological trials are generally shorter than the expected duration of obesity treatment. Pediatric stimulant studies involving loss-of-control eating are uncontrolled and extremely small, while adult BED findings remain translational; neither can establish pediatric treatment efficacy.

Future trials should determine which combinations of behavioral, family, psychological, and pharmacological components work for specific clinical phenotypes. Studies involving obesity and ADHD should prospectively evaluate treatment engagement, executive functioning, eating behavior, growth, body composition, and cardiometabolic outcomes rather than relying on post hoc BMI analyses. Pharmacotherapy studies require longer follow-up through puberty and after discontinuation and should include patients with psychiatric and neurodevelopmental comorbidity who more closely resemble routine clinical populations. The central research question is no longer simply which intervention reduces BMI, but which combination improves metabolic health, psychological well-being, functioning, and long-term participation for a particular child and family.

5. Conclusions

Intensive family-based, multicomponent behavioral treatment remains the best-supported foundation of pediatric obesity care, particularly when it is sufficiently intensive and feasible for the family. Pharmacotherapy can substantially increase and accelerate average BMI reduction in selected adolescents, but it should be integrated with rather than substituted for behavioral, psychological, and family care. Benefits may diminish after medication withdrawal, underscoring the chronic nature of obesity and the need for an explicit long-term treatment plan. Mental-health and eating-behavior assessment should be systematic without assuming that every child with obesity has a psychiatric disorder. In selected patients, unrecognized emotional distress, loss-of-control eating, ADHD, or executive-function difficulties may impair engagement or limit the durability of a weight-directed intervention. Recurrence is therefore more plausibly understood as the result of interacting biological, behavioral, environmental, and sometimes psychological mechanisms than as simple treatment failure or lack of motivation. Treatment success should extend beyond BMI to metabolic health, eating regulation, psychological well-being, family functioning, participation, and sustained outcomes. The most defensible model is phenotype-informed, multidisciplinary, and longitudinal.