1.OBESITY: AN OVERVIEW 1.1 Childhood obesity definition and classification Childhood obesity is a complex, multifactorial, ongoing medical condition characterized by an excessive accumulation of body fat that negatively impacts health general and increase the risk of numerous physical, psychological and metabolic impacts over the lifespan. Its fast-rising incidence and relationship with early onset of non-communicable diseases has made it one of the most urgent public health issues worldwide [8]. Unlike adults, childhood obesity cannot be defined using fixed Body Mass Index (BMI) cut-off values, because body composition, including fat mass and lean body mass, changes constantly with growth and varies according to age and sex. Therefore, BMI in children is assessed in relation to age and sex specific reference standards, rather than as an absolute BMI score. The Body Mass Index (BMI) is the weight in kilograms divided by the square of height in meters (kg/m²) and remains the most widely accepted and practical screening measurement to assess overweight and obesity in children. Although BMI is not a direct measure of body fatness, it has a strong association with adiposity at the population level and is affordable, reliable, and convenient to implement in clinical practice and epidemiological research [8,30]. For children 2 years of age and older, BMI is expressed as a percentile for age and sex based on standardized growth charts. According to the Centers for Disease Control and Prevention (CDC) and the American Academy of Pediatrics (AAP), BMI-for-age percentiles are used to classify weight status into underweight, healthy weight, overweight, and three classes of obesity. This classification facilitates early detection of excessive weight gain, enables timely implementation of preventive and therapeutic interventions, and supports consistent monitoring of growth and obesity trends in both clinical practice and public health research [8,34,35]. Weight Status BMI- for-Age Percentile Underweight < 5th percentile Healthy weight 5th to < 85th percentile Overweight 85th to < 95th percentile Class 1 Obesity ≥ 95th percentile to <120% of the 95th percentile Class 2 Obesity ≥ 120% to < 140% of the 95th percentile Class 3Obesity ≥ 140% of the 95th percentiles Table 1. CDC and APP Classification for childhood obesity Previous terminology such as extreme or morbid obesity has been replaced by the current classification of obesity into Class 1, Class 2 and Class 3. This new nomenclature reflects a person-first, non-stigmatizing language and provides a clinically meaningful assessment of disease severity and to guide appropriate care methods [8,35]. BMI is not usually utilized in children under 2 years of age. The World Health Organization (WHO) suggests using weight-for-length growth norms alternatively to assess obesity since no globally agreed definition for obesity based on BMI has been established for this age group [30,31]. BMI is still the standard screening tool for childhood obesity; however, it is considered an indirect marker of adiposity, not a direct measurement of body fat. Recent evidences underscore the need to define obesity as excessive body fat accumulation, not just increased body weight. In 2025 an international global commission recommended a broader framework for diagnosis, in which BMI should be interpreted with at least one other anthropometric measure (e.g., waist circumference) and evidence of obesity-related organ dysfunction or functional impairment. The committee also established the term preclinical obesity, which are children with excess adiposity but without detectable organ impairment, underlining the need for early identification and appropriate management [21]. 1.2 DIAGNOSTIC CRITERIA OF CHILDOOH OBESITY The diagnosis of pediatric obesity is based mostly on anthropometric assessment, and the Body Mass Index for age is the preferred screening technique for children and adolescents. Compared to adults where fixed BMI threshold is applied irrespective of age and sex, BMI values in children need to be interpreted according to age- and sex- specific growth guidelines, as body composition changes continuously during growth and development. Thus, a BMI score that is considered normal at one age may suggest overweight or obesity at another age, highlighting the need for consistent pediatric growth charts for accurate diagnosis [8,30]. A BMI is calculated by dividing the weight in kilograms by the square of height in meters. In pediatric medicine, calculated BMI is plotted on a standardized growth chart to determine the child’s BMI-for-age percentile or Z score. The method allows clinicians to compare the growth pattern of a single child with a healthy reference group and to detect abnormalities associated with overweight or obesity. Although BMI does not measure body fat directly, it is the most practical, affordable, and reproducible technique for screening excess adiposity in clinical practice and epidemiological investigations[8]. CDC advises the use of BMI-for -age growth charts, issued in 2000, which were created using nationally representative data collected prior to the substantial increase in the prevalence of pediatric obesity. In 2022, the CDC developed the Extended BMI for Age Growth Charts, which more precisely identify extreme obesity. It accurately tracks the BMI levels over 97th percentile and the reference range is extended up to 99.99th percentile. These revised charts can help in the identification and follow-up of children with severe obesity and improve clinical decision making [34,35]. For children <2 years of age, BMI is not frequently used; instead, the CDC recommends an assessment using the World Health Organization (WHO) weight-for-length growth criteria [30,31]. Growth references for several pediatric age groups are accessible from the World Health Organization (WHO) for worldwide use. The WHO Child Growth Standards for children aged 0-5 years were based on healthy children living in optimal environmental and nutritional conditions in six countries: Brazil, Ghana, India, Norway, Oman and the United States. These criteria outline how children should grow in an ideal situation and define overweight as weight-for-length or BMI-for-age > +2 standard deviations (SD) above the median and obesity as > +3 SD [30]. The WHO Growth Reference for children and adolescents aged 5-19 years recommends the use of BMI-for-age Z-scores, with overweight defined as BMI-for-age >+1 SD and obesity as BMI-for-age >+2 SD, relative to the reference population. The WHO reference has been widely used in global public health surveillance, and forms the basis to compare the prevalence of pediatric obesity between countries and populations [30]. Another internationally recognized diagnostic method is that of the International Obesity Task Force (IOTF). The IOTF age- and sex-specific BMI cut-off values were originally determined by Cole and colleagues using nationally representative datasets from six countries and then modified by Cole and Lobstein. These cut-offs are mathematically connected to the adult BMI cut-offs of 25 kg/m2 for overweight and 30 kg/m2 for obesity at 18 years, and so are particularly relevant for international epidemiological studies and for making comparisons between populations. However, multiple studies have shown that the IOTF criteria tend to underestimate the prevalence of pediatric obesity compared to the WHO and CDC guidelines, especially among younger children [10,12]. Although several international organizations advocate slightly different diagnostic criteria, they all agree that BMI values should be evaluated according to age, sex, growth patterns and, when necessary, other anthropometric measurements. Early identification of children at risk, timely management and prevention of obesity-related problems throughout childhood and adulthood can be achieved through accurate diagnosis utilizing standardized growth benchmarks [8,30]. 1.3 GLOBAL PREVALENCE AND TRENDS Childhood obesity has emerged as one of the fastest growing public health challenges worldwide. In both industrialized and developing countries, the frequency of excess body weight among children and adolescents has been increasing steadily over the past decades. Therefore, childhood obesity is now considered to be a substantial contributor to the worldwide burden of non-communicable diseases and has become a focus for international public health organizations [10,18]. According to the data collected from world health organization, since 1990 there is a drastic increase of overweight and obesity in children and adolescents. In 2022, there were more than 390 million children and adolescents aged 5-19 years living with overweight, of which more than 160 million had obesity. In 2024, almost 35 million children under five years of age were living with overweight. In 1990 8% of the world’s children and adolescents were overweight or obese, by 2022 this had increased to 20%. The prevalence of obesity alone increased from 2% to 8% in the same period. An investigation by the NCD Risk Factor Collaboration showed a continuous increase in obesity prevalence in both sexes. After correction for age, global obesity prevalence in females aged 5–19 years rose from 1.7% in 1990 to 6.9% in 2022, and in boys it rose from 2.1% to 9.3% over the same period. Such observations imply that childhood obesity is emerging as a global epidemic that is impacting both sexes with a more pronounced increase observed among boys [18,37]. High-income countries were first to be affected, but current evidence suggests that low- and middle-income countries are experiencing the highest rises in childhood obesity. Many of these countries are currently dealing with the combined burden of malnutrition where obesity coexists with undernutrition and micronutrient deficiencies. This phenomenon presents major issues for healthcare systems as both forms of malnutrition require separate preventive and treatment measures while coexisting in the same populations and, in certain situations, in the same families [31,39] Recent global estimates show that the burden of childhood obesity will continue to rise unless effective prevention strategies are pursued. Analyses published in The Lancet suggest that by 2050 about a third of children and adolescents in the world could be overweight or obese. Such projections highlight the critical need for comprehensive strategies, including healthier school food environments, promotion of physical activity, early identification of children at risk, education of parents, and supportive public health policies to limit children’s exposure to obesogenic environments [6,32]. This problem has worsened in many countries because of the COVID-19 epidemic. School closures, restrictions on outdoor activities, increased screen time, changes in daily routines and dietary habits led to excessive weight gain in children and adolescents. These observations highlighted the need of upholding healthy lifestyles even in times of social instability and showed the necessity for effective public health policies designed to protect children’s nutritional health in shifting circumstances [3,28]. Overall, the evidence available suggests that childhood obesity has become a global epidemic with important medical, social and economic effects. The determinants of effectiveness in prevention go beyond human behaviour and include environmental, educational, socioeconomic and policy-related elements requiring coordinated action of health professionals, families, schools, communities and governments. Strengthening monitoring systems, encouraging healthy lifestyles from early childhood, and implementing evidence-based preventive strategies are critical to reduce the future burden of obesity and its associated problems [29,32,40].

1.4 REGIONAL EPIDEMIOLOGY Childhood obesity is a growing public health problem in the European and Asian nations. The prevalence and associated causes varied between nations, although in most countries the increase in childhood overweight and obesity has been linked to changes in lifestyle and nutrition, urbanization and socioeconomic factors. Moldova and India display two distinct epidemiological patterns: Moldova mirrors the increasing obesity burden in the European region whereas India is facing a dual burden of malnutrition with rising obesity coexisting with persisting undernutrition. Childhood Obesity in the Republic of Moldova The Republic of Moldova is showing a higher prevalence of childhood obesity and overweight, in line with data across the WHO European Region. The WHO European Childhood Obesity Surveillance Initiate (COSI) sixth round 2022-2024 shows that with the data around 470000 children aged 6-9 years are of excess weight and a major health problem from 37 European countries. Almost 25% of children 7-9 years in Europe were overweight including obesity and 11% lived with obesity, with significant differences between nations [41,42]. Moldova takes part in the COSI surveillance programme which allows to assess nationwide changes in the nutritional condition of children. The latest data of Moldovan youngsters show that high body weight is a major health problem among school-age children. In the sixth cycle of surveillance, approximately one in five (20.7%) of the seven-year-old children tested were classed as overweight, including 8.8% obese. The data show that despite the reduced prevalence rates compared to some European nations, childhood excess weight is still a significant public health issue that needs preventive actions[41]. A national survey of 7-year-old children in Moldova found that about one in five youngsters was overweight. In contrast, boys 21.4% were overweight and 9.9% were obese, whereas for girls 20.0% were overweight and 7.5% were obese. Urban children had a higher prevalence than rural children, with overweight 23.7% against 16.0% and obesity 8.2% in comparison to 4.8%, respectively [41]. Another recognised risk that is common in Moldova is the inadequate detection of excess weight by parents. The main reason for the delayed diagnosis and interventions is the misunderstanding of the parents because more than 70 % of the overweight children were seen as normal by their parents. The dietary pattern also plays an important role in obesity. In youngsters, regular consumption of sugary snacks is common, while only a tiny number of children consume the necessary number of fruits and vegetables [41]. Moldova has addressed this increasing problem by including the prevention of childhood obesity in public health programs. The National Programme for Prevention and Control of Non-Communicable Diseases 2023–2027 outlines measures to promote good nutrition, improve food environments in schools and prevent further rise of obesity in youth [17]. Childhood Obesity in India The epidemiological picture in India is distinctive with a dual burden of malnutrition, i.e., co-existence of undernutrition with growing childhood obesity. Undernutrition continues to be a problem for many rural and poor populations, while childhood overweight and obesity are growing fast, particularly in metropolitan areas and in higher socioeconomic categories [20,39]. The rise of obesity in Indian youngsters has been associated with urbanization, changing food preferences, greater consumption of processed foods, less physical exercise and increased sedentary behaviour. These factors have led to a switch from traditional diets to higher calorie foods, which increases the risk of excessive weight gain among children and adolescents [9,20]. Between the years of 1995 and 2023 , it found that the increased incidence of obesity among Indian school-aged children to be 6,97% by systematic review and meta-analysis conducted on 125 studies.( 95% Cl: 5.97-7.97%) [10]Prevalence was equal in boys and girls with obesity rates of about 6.37 percent in both sexes. However, there were large regional variations with the highest frequency being reported from Arunachal Pradesh (17.92%) and Delhi (13.57%) and lower rates from locations like Manipur. Central India had a prevalence of 5.63% and North India had the greatest regional frequency (8.58%) [36]. Studies in urban areas have revealed considerably greater rates of overweight and obesity in childhood. For instance, a study of school-going children in Lucknow using Indian Academy of Pediatrics (IAP) standards reported a combined incidence of overweight and obesity of 29.7% indicating the impact of urbanization on lifestyle and childhood health [20]. The Indian Academy of Pediatrics Revised Guidelines 2023 highlight that the majority of pediatric obesity in India is associated with environmental and lifestyle factors and not secondary medical causes. The guidelines point to overeating of high-calorie foods, lack of exercise, screen time and genetic predisposition as important causes. The typical “thin-fat Indian phenotype” with greater central adiposity in spite of relatively lower BMI values further raises the risk of metabolic problems, which needs to be identified early and managed [9]. In conclusion, childhood obesity is becoming a great health concern both in Moldova and India. Regardless of the disparities in socio-economic situations and nutritional patterns, both countries need robust monitoring systems, early diagnosis, nutrition education and preventive measures to lessen the future burden of obesity related disorders. 1.5 PUBLIC HEALTH SIGNIFICANCE OF PEDIATRIC OBESITY The increasing frequency of pediatric obesity and its association with multiple physical, psychological, and economic implications, makes it one of the major public health problems worldwide. Childhood overweight harms normal growth and development and significantly raises the risk of chronic non-communicable diseases in later life. Since many consequences of obesity begin in childhood and carry on into adulthood, early detection and prevention have become important priorities for healthcare systems globally [10,18,23]. Immediate Health Consequences Childhood obesity is related with various comorbidities across almost all organ systems. Among the most common are metabolic problems. Obesity-mediated insulin resistance has caused a dramatic increase in type 2 diabetes mellitus (T2DM) among children and adolescents, which used to be rare in the pediatric population [17,20]. Obese children also typically suffer from metabolic syndrome, which is defined by abdominal obesity, hypertension, dyslipidemia and impaired glucose metabolism. A recent comprehensive study found a median prevalence of 26.9% and 5.5% in low- and middle-income and high-income countries, respectively [1,8]. Metabolic dysfunction-associated steatotic liver disease (MASLD), previously referred to as non-alcoholic fatty liver disease (NAFLD), is another significant metabolic consequence. Approximately 47.5 % of obese youngsters in middle-income nations and 23 % in high-income countries are impacted. Dyslipidemia (increased triglycerides and decreased high-density lipoprotein cholesterol) is also frequent, found in 43.5%–73.7% of children with obesity [8,10]. Cardiovascular problems occur in early childhood. Hypertension is found in about 35.6% of obese children in low- and middle-income countries compared to 12.7% in high-income countries. Moreover, studies have revealed endothelial dysfunction, increased carotid intima-media thickness and early atherosclerotic alterations in obese children, demonstrating that cardiovascular disease begins long before adult age. These cardiovascular risk factors often continue throughout life and considerably raise the risk of future cardiovascular disease [2,11]. Endocrine problems include polycystic ovarian syndrome (PCOS) in teenage girls, central precocious puberty, and abnormalities of thyroid and adrenal function. Respiratory diseases such as obstructive sleep apnea and exercise intolerance are also frequent, resulting in poor sleep quality and limited physical activity. Moreover, orthopedic disorders such as Blount disease, slipping capital femoral epiphysis and pes planus are more common in obese individuals. Neurological consequences such as idiopathic intracranial hypertension can be seen in some severe cases [8,12,25]. Long Term Consequences Tracking of obesity from childhood to adulthood is one of the most critical public health implications. Approximately 84% of children with BMI between the 95th and 98th percentiles develop obesity in adulthood with BMI >30 kg/m2. Childhood-established obesity, hypertension, dyslipidemia and insulin resistance are independent predictors of adult cardiovascular disease and premature death, and have been demonstrated in longitudinal investigations [5,11,23]. If not effectively intervened, children with obesity are at much higher risk for developing type 2 diabetes mellitus, coronary artery disease, stroke, chronic renal disease, osteoarthritis, and several obesity-related malignancies in adulthood. Therefore, prevention and early treatment in children provide a crucial opportunity to lessen the future burden of chronic disease [11,23,29]. Psychological and Social Impact Childhood obesity includes physical health concerns as well as serious psychological and social repercussions. Children with obesity have been reported to have greater rates of sadness, anxiety, low self-esteem, and negative body image than children with healthy weight. They are also more prone to weight-based stigma, bullying and social exclusion, which severely influence academic achievement, interpersonal relationships and general quality of life. Emotional strain can additionally cause poor eating choices and decreased physical activity, which causes a self reinforcing cycle that worsens obesity [8,10]. Economic Burden Childhood obesity carries a significant financial cost for individuals, health care systems and society. Direct healthcare costs include charges of medical consultations, diagnostic investigations and treatment of obesity-related disorders including diabetes, hypertension and liver disease. Lower educational attainment, less output, disability and early death later in life are the indirect costs. As more fat children grow into adults with chronic disease, health costs continue to increase. Investment in obesity prevention and early intervention is thus not only a public health priority but also a cost-effective strategy to reduce future health care expenditures and improve population health outcomes [29,32,40].

1.6 ETIOLOGY AND PATHOPHYSIOLOGY OF OBESITY IN CHILDREN Childhood obesity is a complex, chronic and multifactorial disease that is the result of the interaction of genetic susceptibility, neuroendocrine mechanisms, metabolic processes, early-life exposures, behavioural factors and the wider physical and socioeconomic environment. Excessive energy intake relative to energy expenditure is a crucial mechanism yet obesity cannot be explained by individual dietary choices or physical inactivity alone. Instead, genetic and biological susceptibility combines with an increasingly obesogenic environment to impair the control of hunger, energy expenditure, adipose tissue function and metabolic balance [8,10,19]. Classification According to the Etiology Childhood obesity is classified into primary (exogenous or multifactorial) and secondary (endogenous) obesity. Most cases of primary obesity are due to the interaction between genetic predisposition and environmental and behavioural factors, including excessive energy intake, reduced physical activity, sedentary behaviour, inadequate sleep and exposure to an obesogenic food environment [8,10] Secondary obesity is less common and occurs as a result of an identifiable underlying disorder, genetic condition or medication exposure. Endocrine causes include hypothyroidism, Cushing syndrome, and growth hormone insufficiency. Genetic reasons include syndromic illnesses such as Prader–Willi, Bardet–Biedl and Alstrom syndromes, and monogenic versions with defects in the leptin–melanocortin system, including the LEP, LEPR, POMC and MC4R genes. [8,13,19]. Hypothalamic obesity may develop after hypothalamic damage due to craniopharyngioma, neurosurgery, radiotherapy or traumatic brain injury. Also, some medications like systemic corticosteroids and some psychotropic and antiepileptic medications can cause weight gain [8,12,25]. Secondary obesity should be suspected in the presence of clinical symptoms such as severe or rapidly developing obesity at a very young age, decreased linear growth, developmental delay, dysmorphic features, considerable hyperphagia or poor response to recommended lifestyle changes. However, primary and secondary factors can occur together and environmental factors can alter the severity of obesity even in children with a genetic or endocrine disorder underlying [8,13]. Energy Balance and Neuroendocrine Regulations The central physiological mechanism of obesity is a sustained positive energy balance, in which energy intake exceeds energy expenditure over time. Energy homeostasis is regulated by interactions between peripheral signals originating from adipose tissue, the gastrointestinal tract and pancreas and central pathways located mainly in the hypothalamus [10,12]. Two major neural systems in the hypothalamus are involved in the control of appetite, located in the arcuate nucleus. Pro-opiomelanocortin (POMC) neurons secrete α-melanocyte-stimulating hormone that activates melanocortin-4 receptors (MC4R) to increase satiety. In contrast, neurons expressing neuropeptide Y and agouti-related peptide enhance food intake and energy conservation. Hormones, such as leptin, insulin and ghrelin, alter the equilibrium between these pathways [12,19]. Adipocytes release leptin in accordance to body fat levels, which ordinarily operates on the hypothalamus to decrease food intake and increase energy expenditure. In the common form of obesity, levels of leptin are high but the response of the central nervous system to leptin is defective, resulting in leptin resistance. Thus, the increased stores of fat do not result in the expected decrease in appetite. Ghrelin is a key orexigenic hormone which is produced mainly by the stomach. Normally it increases before meals and decreases after eating. Persistent hunger and increased energy intake may result from changes in appetite regulation and postprandial hormonal responses [19,12]. Sleep is an important regulator of energy homeostasis . In children, insufficient or irregular sleep may have adverse effects on appetite regulation, increase hunger and preference for energy dense foods and promote sedentary activity. These effects may contribute to excess weight gain over time [6,24]. Genetic and Epigenetic Factors The development of childhood obesity is influenced by the genetic predisposition. The majority of cases are polygenic, with multiple genetic variants underlying differences in appetite regulation, food reward, adipocyte development, energy expenditure and glucose and lipid metabolism. Rare mutations in the leptin–melanocortin pathway can induce severe, early-onset monogenic obesity, sometimes with severe hyperphagia [16,13,19]. Early childhood environmental exposures are linked to subsequent risk of obesity through epigenetic pathways. Changes in gene expression can occur without alteration of the DNA sequence through DNA methylation, histone modifications, and non-coding RNAs. These processes may be modulated by maternal obesity, gestational diabetes, excessive gestational weight gain, fetal growth restriction, rapid post-natal catch-up growth, early nutrition and exposure to endocrine-disrupting chemicals [7,27]. Children born small for gestational age, who then undergo rapid catch-up growth, may be at increased risk for subsequent obesity and metabolic disease. This connection is believed to entail embryonic programming, altered insulin sensitivity, adipose tissue development and epigenetic control [7,27]. Thus, predisposition to childhood obesity may begin in the perinatal period and continue to be influenced by environmental circumstances throughout early life. Adipose Tissue Dysfunction and Chronic Inflammation Adipose tissue is an active endocrine and immune organ. Excessive weight gain leads to adipocyte hypertrophy and cellular stress, resulting in adipose tissue malfunction and low-grade chronic inflammation [22]. Obesity is related with increased production of pro-inflammatory mediators such as tumour necrosis factor-alpha and interleukin-6, whereas the adiponectin concentration, an anti-inflammatory and insulin-sensitizing adipokine, is generally decreased [22]. There are also a higher recruitment and activation of immune cells, notably macrophages, that further enhances the inflammatory signaling in adipose tissue. These mechanisms interfere with insulin signaling in adipose tissue, skeletal muscle and liver and contribute to systemic insulin resistance. Hyperinsulinaemia and insulin resistance then lead to metabolic derangements such as abnormal lipid metabolism and increased risk of metabolic dysfunction-associated steatotic liver disease and type 2 diabetes mellitus [8,22]. Role of Gut Microbiome The gut microbiota is an emerging element in the pathogenesis of pediatric obesity. Changes in the composition and behavior of intestinal bacteria, termed dysbiosis, may affect energy metabolism, intestinal barrier function, immunological responses and systemic inflammation [33]. Gut bacteria digest food constituents and create short-chain fatty acids such as acetate, propionate and butyrate. These metabolites can alter energy metabolism and increase the release of gastrointestinal hormones, such as glucagon-like peptide-1 and peptide YY, that play a role in hunger and glucose regulation [33]. However, the association between the gut microbiota and obesity is complex, impacted by diet, age, antibiotic exposure, geography and socioeconomic factors. Thus, simple bacterial patterns such an increased Firmicutes-to-Bacteroidetes ratio cannot be viewed as a universal marker or independent cause of obesity at now [33]. Environmental, Behavioural and Socioeconomic Determinants The development of childhood obesity in an ever more obesogenic environment. Dietary variables include increased consumption of ultra-processed meals, sugar-sweetened beverages, fast food, energy-dense foods with low nutritional value and inadequate intake of fruits, vegetables, whole grains and dietary fibre [10,37]. Reduced physical activity and increased sedentary behaviour also contribute to positive energy balance. Urbanization, less active commuting, limited access to safe recreational spaces and decreased opportunities for outdoor play may decrease daily energy expenditure. Screen time may also be associated with sedentary behaviour, sleep disruption and exposure to marketing of energy-dense meals and sugar-sweetened beverages [24,37]. Socioeconomic factors affect the risk of obesity through access to nutritious food, education, housing, neighbourhood safety and recreation facilities. In many high-income countries, childhood obesity is more common in socioeconomically disadvantaged groups, whereas in some low- and middle-income countries obesity may initially be more common in higher-income urban populations and then gradually shift towards disadvantaged populations during the nutrition transition [10,31]. Parental obesity is a powerful predictor of offspring obesity because of the combined impact of genetic vulnerability and shared family settings. Parental feeding practices, the availability of food in the home, and family patterns of eating and physical activity can be important in the risk of childhood obesity [5,10].Prenatal variables such as maternal obesity, gestational diabetes and excess gestational weight gain are also associated with higher risk of obesity in offspring and may act via metabolic, hormonal, microbiome-related and epigenetic processes [7,27]. In summary, childhood obesity is the consequence of the complex interaction between genetic predisposition, neuroendocrine regulation, adipose tissue malfunction, early-life programming, gut microbiome changes, nutrition, physical activity, sleep and socioeconomic situations. This multifactorial model demonstrates that childhood obesity is not a consequence of individual lifestyle choices, but a complex chronic disease that requires integrated prevention and management at the individual, family, healthcare and population levels [8,10,40].

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