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Review article, childhood and adolescent obesity: a review.

• 1 Division of Endocrinology, Diabetes and Metabolism, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, United States
• 2 Division of Adolescent Medicine, Department of Pediatrics, Medical College of Wisconsin Affiliated Hospitals, Milwaukee, WI, United States
• 3 Division of Adolescent Medicine, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, United States

Obesity is a complex condition that interweaves biological, developmental, environmental, behavioral, and genetic factors; it is a significant public health problem. The most common cause of obesity throughout childhood and adolescence is an inequity in energy balance; that is, excess caloric intake without appropriate caloric expenditure. Adiposity rebound (AR) in early childhood is a risk factor for obesity in adolescence and adulthood. The increasing prevalence of childhood and adolescent obesity is associated with a rise in comorbidities previously identified in the adult population, such as Type 2 Diabetes Mellitus, Hypertension, Non-alcoholic Fatty Liver disease (NAFLD), Obstructive Sleep Apnea (OSA), and Dyslipidemia. Due to the lack of a single treatment option to address obesity, clinicians have generally relied on counseling dietary changes and exercise. Due to psychosocial issues that may accompany adolescence regarding body habitus, this approach can have negative results. Teens can develop unhealthy eating habits that result in Bulimia Nervosa (BN), Binge- Eating Disorder (BED), or Night eating syndrome (NES). Others can develop Anorexia Nervosa (AN) as they attempt to restrict their diet and overshoot their goal of “being healthy.” To date, lifestyle interventions have shown only modest effects on weight loss. Emerging findings from basic science as well as interventional drug trials utilizing GLP-1 agonists have demonstrated success in effective weight loss in obese adults, adolescents, and pediatric patients. However, there is limited data on the efficacy and safety of other weight-loss medications in children and adolescents. Nearly 6% of adolescents in the United States are severely obese and bariatric surgery as a treatment consideration will be discussed. In summary, this paper will overview the pathophysiology, clinical, and psychological implications, and treatment options available for obese pediatric and adolescent patients.

Introduction

Obesity is a complex issue that affects children across all age groups ( 1 – 3 ). One-third of children and adolescents in the United States are classified as either overweight or obese. There is no single element causing this epidemic, but obesity is due to complex interactions between biological, developmental, behavioral, genetic, and environmental factors ( 4 ). The role of epigenetics and the gut microbiome, as well as intrauterine and intergenerational effects, have recently emerged as contributing factors to the obesity epidemic ( 5 , 6 ). Other factors including small for gestational age (SGA) status at birth, formula rather than breast feeding in infancy, and early introduction of protein in infant's dietary intake have been reportedly associated with weight gain that can persist later in life ( 6 – 8 ). The rising prevalence of childhood obesity poses a significant public health challenge by increasing the burden of chronic non-communicable diseases ( 1 , 9 ).

Obesity increases the risk of developing early puberty in children ( 10 ), menstrual irregularities in adolescent girls ( 1 , 11 ), sleep disorders such as obstructive sleep apnea (OSA) ( 1 , 12 ), cardiovascular risk factors that include Prediabetes, Type 2 Diabetes, High Cholesterol levels, Hypertension, NAFLD, and Metabolic syndrome ( 1 , 2 ). Additionally, obese children and adolescents can suffer from psychological issues such as depression, anxiety, poor self-esteem, body image and peer relationships, and eating disorders ( 13 , 14 ).

So far, interventions for overweight/obesity prevention have mainly focused on behavioral changes in an individual such as increasing daily physical exercise or improving quality of diet with restricting excess calorie intake ( 1 , 15 , 16 ). However, these efforts have had limited results. In addition to behavioral and dietary recommendations, changes in the community-based environment such as promotion of healthy food choices by taxing unhealthy foods ( 17 ), improving lunch food quality and increasing daily physical activity at school and childcare centers, are extra measures that are needed ( 16 ). These interventions may include a ban on unhealthy food advertisements aimed at children as well as access to playgrounds and green spaces where families can feel their children can safely recreate. Also, this will limit screen time for adolescents as well as younger children.

However, even with the above changes, pharmacotherapy and/or bariatric surgery will likely remain a necessary option for those youth with morbid obesity ( 1 ). This review summarizes our current understanding of the factors associated with obesity, the physiological and psychological effects of obesity on children and adolescents, and intervention strategies that may prevent future concomitant issues.

Definition of Childhood Obesity

Body mass index (BMI) is an inexpensive method to assess body fat and is derived from a formula derived from height and weight in children over 2 years of age ( 1 , 18 , 19 ). Although more sophisticated methods exist that can determine body fat directly, they are costly and not readily available. These methods include measuring skinfold thickness with a caliper, Bioelectrical impedance, Hydro densitometry, Dual-energy X-ray Absorptiometry (DEXA), and Air Displacement Plethysmography ( 2 ).

BMI provides a reasonable estimate of body fat indirectly in the healthy pediatric population and studies have shown that BMI correlates with body fat and future health risks ( 18 ). Unlike in adults, Z-scores or percentiles are used to represent BMI in children and vary with the age and sex of the child. BMI Z-score cut off points of >1.0, >2.0, and >3.0 are recommended by the World Health Organization (WHO) to define at risk of overweight, overweight and obesity, respectively ( 19 ). However, in terms of percentiles, overweight is applied when BMI is >85th percentile <95th percentile, whereas obesity is BMI > 95th percentile ( 20 – 22 ). Although BMI Z-scores can be converted to BMI percentiles, the percentiles need to be rounded and can misclassify some normal-weight children in the under or overweight category ( 19 ). Therefore, to prevent these inaccuracies and for easier understanding, it is recommended that the BMI Z-scores in children should be used in research whereas BMI percentiles are best used in the clinical settings ( 20 ).

As BMI does not directly measure body fat, it is an excellent screening method, but should not be used solely for diagnostic purposes ( 23 ). Using 85th percentile as a cut off point for healthy weight may miss an opportunity to obtain crucial information on diet, physical activity, and family history. Once this information is obtained, it may allow the provider an opportunity to offer appropriate anticipatory guidance to the families.

Pathophysiology of Obesity

The pathophysiology of obesity is complex that results from a combination of individual and societal factors. At the individual level, biological, and physiological factors in the presence of ones' own genetic risk influence eating behaviors and tendency to gain weight ( 1 ). Societal factors include influence of the family, community and socio-economic resources that further shape these behaviors ( Figure 1 ) ( 3 , 24 ).

Figure 1 . Multidimensional factors contributing to child and adolescent obesity.

Biological Factors

There is a complex architecture of neural and hormonal regulatory control, the Gut-Brain axis, which plays a significant role in hunger and satiety ( Figure 2 ). Sensory stimulation (smell, sight, and taste), gastrointestinal signals (peptides, neural signals), and circulating hormones further contribute to food intake ( 25 – 27 ).

Figure 2 . Pictorial representation of the Hunger-Satiety pathway a and the various hormones b involved in the pathway. a, Y1/Y5R and MC3/4 are second order neuro receptors which are responsible in either the hunger or satiety pathway. Neurons in the ARC include: NPY, Neuropeptide Y; AgRP, Agouti-Related Peptide; POMC, Pro-Opiomelanocortin; CART, Cocaine-and Amphetamine-regulated Transcript; α-MSH, α-Melanocyte Stimulating Hormone. b, PYY, Peptide YY; PP, Pancreatic Polypeptide; GLP-1, Glucagon-Like Peptide- I; OMX, Oxyntomodulin.

The hypothalamus is the crucial region in the brain that regulates appetite and is controlled by key hormones. Ghrelin, a hunger-stimulating (orexigenic) hormone, is mainly released from the stomach. On the other hand, leptin is primarily secreted from adipose tissue and serves as a signal for the brain regarding the body's energy stores and functions as an appetite -suppressing (anorexigenic) hormone. Several other appetite-suppressing (anorexigenic) hormones are released from the pancreas and gut in response to food intake and reach the hypothalamus through the brain-blood barrier (BBB) ( 28 – 32 ). These anorexigenic and orexigenic hormones regulate energy balance by stimulating hunger and satiety by expression of various signaling pathways in the arcuate nucleus (ARC) of the hypothalamus ( Figure 2 ) ( 28 , 33 ). Dysregulation of appetite due to blunted suppression or loss of caloric sensing signals can result in obesity and its morbidities ( 34 ).

Emotional dysfunction due to psychiatric disorders can cause stress and an abnormal sleep-wake cycles. These modifications in biological rhythms can result in increased appetite, mainly due to ghrelin, and can contribute to emotional eating ( 35 ).

Recently, the role of changes in the gut microbiome with increased weight gain through several pathways has been described in literature ( 36 , 37 ). The human gut serves as a host to trillions of microorganisms, referred to as gut microbiota. The dominant gut microbial phyla are Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria, Fusobacteria, and Verrucomicrobia, with Firmicutes and Bacteroidetes representing 90% of human gut microbiota ( 5 , 38 ). The microbes in the gut have a symbiotic relationship within their human host and provide a nutrient-rich environment. Gut microbiota can be affected by various factors that include gestational age at birth, mode of infant delivery, type of neonatal and infant feeding, introduction of solid food, feeding practices and external factors like antibiotic use ( 5 , 38 ). Also, the maturation of the bacterial phyla that occurs from birth to adulthood ( 39 ), is influenced by genetics, environment, diet, lifestyle, and gut physiology and stabilizes in adulthood ( 5 , 39 , 40 ). Gut microbiota is unique to each individual and plays a specific role in maintaining structural integrity, and the mucosal barrier of the gut, nutrient metabolism, immune response, and protection against pathogens ( 5 , 37 , 38 ). In addition, the microbiota ferments the indigestible food and synthesizes other essential micronutrients as well as short chain fatty acids (SCFAs') ( 40 , 41 ). Dysbiosis or imbalance of the gut microbiota, in particularly the role of SCFA has been linked with the patho-physiology of obesity ( 36 , 38 , 41 , 42 ). SCFAs' are produced by anaerobic fermentation of dietary fiber and indigestible starch and play a role in mammalian energy metabolism by influencing gut-brain communication axis. Emerging evidence has shown that increased ratio of Firmicutes to Bacteroidetes causes increased energy extraction of calories from diets and is evidenced by increased production of short chain fatty acids (SCFAs') ( 43 – 45 ). However, this relationship is not affirmed yet, as a negative relationship between SCFA levels and obesity has also been reported ( 46 ). Due to the conflicting data, additional randomized control trials are needed to clarify the role of SCFA's in obese and non-obese individuals.

The gut microbiota also has a bidirectional interaction with the liver, and various additional factors such as diet, genetics, and the environment play a key role in this relationship. The Gut- Liver Axis is interconnected at various levels that include the mucus barrier, epithelial barrier, and gut microbiome and are essential to maintain normal homeostasis ( 47 ). Increased intestinal mucosal permeability can disrupt the gut-liver axis, which releases various inflammatory markers, activates an innate immune response in the liver, and results in a spectrum of liver diseases that include hepatic steatosis, non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC) ( 48 , 49 ).

Other medical conditions, including type 2 Diabetes Mellitus, Metabolic Syndrome, eating disorders as well as psychological conditions such as anxiety and depression are associated with the gut microbiome ( 50 – 53 ).

Genetic Factors

Genetic causes of obesity can either be monogenic or polygenic types. Monogenic obesity is rare, mainly due to mutations in genes within the leptin/melanocortin pathway in the hypothalamus that is essential for the regulation of food intake/satiety, body weight, and energy metabolism ( 54 ). Leptin regulates eating behaviors, the onset of puberty, and T-cell immunity ( 55 ). About 3% of obese children have mutations in the leptin ( LEP ) gene and the leptin receptor (LEPR) and can also present with delayed puberty and immune dysfunction ( 55 , 56 ). Obesity caused by other genetic mutations in the leptin-melanocortin pathway include proopiomelanocortin (POMC) and melanocortin receptor 4 (MC4R), brain-derived neurotrophic factor (BDNF), and the tyrosine kinase receptor B (NTRK2) genes ( 57 , 58 ). Patients with monogenic forms generally present during early childhood (by 2 years old) with severe obesity and abnormal feeding behaviors ( 59 ). Other genetic causes of severe obesity are Prader Willi Syndrome (PWS), Alström syndrome, Bardet Biedl syndrome. Patients with these syndromes present with additional characteristics, including cognitive impairment, dysmorphic features, and organ-specific developmental abnormalities ( 60 ). Individuals who present with obesity, developmental delay, dysmorphic features, and organ dysfunction should receive a genetics referral for further evaluation.

Polygenic obesity is the more common form of obesity, caused by the combined effect of multiple genetic variants. It is the result of the interplay between genetic susceptibility and the environment, also known as the Gene-Environment Interaction (GEI) ( 61 – 64 ). Genome-wide association studies (GWAS) have identified gene variants [single nucleotide polymorphism (SNPs)] for body mass index (BMI) that likely act synergistically to affect body weight ( 65 ). Studies have identified genetic variants in several genes that may contribute to excessive weight gain by increasing hunger and food intake ( 66 – 68 ). When the genotype of an individual confers risk for obesity, exposure to an obesogenic environment may promote a state of energy imbalance due to behaviors that contribute to conserving rather than expending energy ( 69 , 70 ). Research studies have shown that obese individuals have a genetic variation that can influence their actions, such as increased food intake, lack of physical activity, a decreased metabolism, as well as an increased tendency to store body fat ( 63 , 66 , 67 , 69 , 70 ).

Recently the role of epigenetic factors in the development of obesity has emerged ( 71 ). The epigenetic phenomenon may alter gene expression without changing the underlying DNA sequence. In effect, epigenetic changes may result in the addition of chemical tags known as methyl groups, to the individual's chromosomes. This alteration can result in a phenomenon where critical genes are primed to on and off regulate. Complex physiological and psychological adjustment occur during infancy and can thereafter set the stage for health vs. disease. Developmental origins of health and disease (DOHaD) shows that early life environment can impact the risk of chronic diseases later in life due to fetal programming secondary to epigenetic changes ( 72 ). Maternal nutrition during the prenatal or early postnatal period may trigger these epigenetic changes and increase the risk for chronic conditions such as obesity, metabolic and cardiovascular disease due to epigenetic modifications that may persist and cause intergenerational effect on the health children and adults ( 58 , 73 , 74 ). Similarly, adverse childhood experiences (ACE) have been linked to a broad range of negative outcomes through epigenetic mechanisms ( 75 ) and promote unhealthy eating behaviors ( 76 , 77 ). Other factors such as diet, physical activity, environmental and psychosocial stressors can cause epigenetic changes and place an individual at risk for weight gain ( 78 ).

Developmental Factors

Eating behaviors evolve over the first few years of life. Young children learn to eat through their direct experience with food and observing others eating around them ( 79 ). During infancy, feeding defines the relationship of security and trust between a child and the parent. Early childhood eating behaviors shift to more self-directed control due to rapid physical, cognitive, communicative, and social development ( 80 ). Parents or caregivers determine the type of food that is made available to the infant and young child. However, due to economic limitations and parents having decreased time to prepare nutritious meals, consumption of processed and cheaper energy-dense foods have occurred in Western countries. Additionally, feeding practices often include providing large or super-sized portions of palatable foods and encouraging children to finish the complete meal (clean their plate even if they do not choose to), as seen across many cultures ( 81 , 82 ). Also, a segment of parents are overly concerned with dietary intake and may pressurize their child to eat what they perceive as a healthy diet, which can lead to unintended consequences ( 83 ). Parents' excessive restriction of food choices may result in poor self-regulation of energy intake by their child or adolescent. This action may inadvertently promote overconsumption of highly palatable restricted foods when available to the child or adolescent outside of parental control with resultant excessive weight gain ( 84 , 85 ).

During middle childhood, children start achieving greater independence, experience broader social networks, and expand their ability to develop more control over their food choices. Changes that occur in the setting of a new environment such as daycare or school allow exposure to different food options, limited physical activity, and often increased sedentary behaviors associated with school schedules ( 24 ). As the transition to adolescence occurs, physical and psychosocial development significantly affect food choices and eating patterns ( 25 ). During the teenage years, more independence and interaction with peers can impact the selection of fast foods that are calorically dense. Moreover, during the adolescent years, more sedentary behaviors such as video and computer use can limit physical exercise. Adolescence is also a period in development with an enhanced focus on appearance, body weight, and other psychological concerns ( 86 , 87 ).

Environmental Factors

Environmental changes within the past few decades, particularly easy access to high-calorie fast foods, increased consumption of sugary beverages, and sedentary lifestyles, are linked with rising obesity ( 88 ). The easy availability of high caloric fast foods, and super-sized portions, are increasingly common choices as individuals prefer these highly palatable and often less expensive foods over fruits and vegetables ( 89 ). The quality of lunches and snacks served in schools and childcare centers has been an area of debate and concern. Children and adolescents consume one-third to one-half of meals in the above settings. Despite policies in place at schools, encouraging foods, beverages, and snacks that are deemed healthier options, the effectiveness of these policies in improving children's dietary habits or change in obesity rate has not yet been seen ( 90 ). This is likely due to the fact that such policies primarily focus on improving dietary quality but not quantity which can impact the overweight or obese youth ( 91 ). Policies to implement taxes on sugary beverages are in effect in a few states in the US ( 92 ) as sugar and sugary beverages are associated with increased weight gain ( 2 , 3 ). This has resulted in reduction in sales of sugary drinks in these states, but the sales of these types of drinks has risen in neighboring states that did not implement the tax ( 93 ). Due to advancements in technology, children are spending increased time on electronic devices, limiting exercise options. Technology advancement is also disrupting the sleep-wake cycle, causing poor sleeping habits, and altered eating patterns ( 94 ). A study published on Canadian children showed that the access to and night-time use of electronic devices causes decreased sleep duration, resulting in excess body weight, inferior diet quality, and lower physical activity levels ( 95 ).

Infant nutrition has gained significant popularity in relation to causing overweight/obesity and other diseases later in life. Breast feeding is frequently discussed as providing protection against developing overweight/obesity in children ( 8 ). Considerable heterogeneity has been observed in studies and conducting randomized clinical trials between breast feeding vs. formula feeding is not feasible ( 8 ). Children fed with a low protein formula like breast milk are shown to have normal weight gain in early childhood as compared to those that are fed formulas with a high protein load ( 96 ). A recent Canadian childbirth cohort study showed that breast feeding within first year of life was inversely associated with weight gain and increased BMI ( 97 ). The effect was stronger if the child was exclusively breast fed directly vs. expressed breast milk or addition of formula or solid food ( 97 ). Also, due to the concern of poor growth in preterm or SGA infants, additional calories are often given for nutritional support in the form of macronutrient supplements. Most of these infants demonstrate “catch up growth.” In fact, there have been reports that in some children the extra nutritional support can increase the risk for overweight/obesity later in life. The association, however, is inconsistent. Recently a systemic review done on randomized controlled trials comparing the studies done in preterm and SGA infants with feeds with and without macronutrient supplements showed that macronutrient supplements may increase weight and length in toddlers but did not show a significant increase in the BMI during childhood ( 98 ). Increased growth velocity due to early introduction of formula milk and protein in infants' diet, may influence the obesity pathways, and can impact fetal programming for metabolic disease later in life ( 99 ).

General pediatricians caring for children with overweight/obesity, generally recommend endocrine testing as parents often believe that there may be an underlying cause for this condition and urge their primary providers to check for conditions such as thyroid abnormalities. Endocrine etiologies for obesity are rarely identified and patients with underlying endocrine disorders causing excessive weight gain usually are accompanied by attenuated growth patterns, such that a patient continues to gain weight with a decline in linear height ( 100 ). Various endocrine etiologies that one could consider in a patient with excessive weight gain in the setting of slow linear growth: severe hypothyroidism, growth hormone deficiency, and Cushing's disease/syndrome ( 58 , 100 ).

Clinical-Physiology of Pediatric Obesity

It is a well-known fact that early AR(increased BMI) before the age of 5 years is a risk factor for adult obesity, obesity-related comorbidities, and metabolic syndrome ( 101 – 103 ). Typically, body mass index (BMI) declines to a minimum in children before it starts increasing again into adulthood, also known as AR. Usually, AR happens between 5 and 7 years of age, but if it occurs before the age of 5 years is considered early AR. Early AR is a marker for higher risk for obesity-related comorbidities. These obesity-related health comorbidities include cardiovascular risk factors (hypertension, dyslipidemia, prediabetes, and type 2 diabetes), hormonal issues, orthopedic problems, sleep apnea, asthma, and fatty liver disease ( Figure 3 ) ( 9 ).

Figure 3 . Obesity related co-morbidities a in children and adolescents. a, NAFLD, Non-Alcoholic Fatty Liver Disease; SCFE, Slipped Capital Femoral Epiphysis; PCOS, Polycystic Ovary Syndrome; OSA, Obstructive Sleep Apnea.

Clinical Comorbidities of Obesity in Children

Growth and puberty.

Excess weight gain in children can influence growth and pubertal development ( 10 ). Childhood obesity can cause prepubertal acceleration of linear growth velocity and advanced bone age in boys and girls ( 104 ). Hyperinsulinemia is a normal physiological state during puberty, but children with obesity can have abnormally high insulin levels ( 105 ). Leptin resistance also occurs in obese individuals who have higher leptin levels produced by their adipose tissue ( 55 , 106 ). The insulin and leptin levels can act on receptors that impact the growth plates with a resultant bone age advancement ( 55 ).

Adequate nutrition is essential for the typical timing and tempo of pubertal onset. Excessive weight gain can initiate early puberty, due to altered hormonal parameters ( 10 ). Obese children may present with premature adrenarche, thelarche, or precocious puberty (PP) ( 107 ). The association of early pubertal changes with obesity is consistent in girls, and is well-reported; however, data is sparse in boys ( 108 ). One US study conducted in racially diverse boys showed obese boys had delayed puberty, whereas overweight boys had early puberty as compared to normal-weight boys ( 109 ). Obese girls with PP have high leptin levels ( 110 , 111 ). Healthy Lifestyle in Europe by Nutrition in Adolescence (HELENA) is a cross-sectional study and suggested an indirect relationship between elevated leptin levels, early puberty, and cardiometabolic and inflammatory markers in obese girls ( 112 ). Additionally, obese girls with premature adrenarche carry a higher risk for developing polycystic ovary syndrome (PCOS) in the future ( 113 , 114 ).

Sleep Disorders

Obesity is an independent risk factor for obstructive sleep apnea (OSA) in children and adolescents ( 12 , 115 ). Children with OSA have less deleterious consequences in terms of cardiovascular stress of metabolic syndrome when compared to adolescents and adults ( 116 , 117 ). In children, abnormal behaviors and neurocognitive dysfunction are the most critical and frequent end-organ morbidities associated with OSA ( 12 ). However, in adolescents, obesity and OSA can independently cause oxidative systemic stress and inflammation ( 118 , 119 ), and when this occurs concurrently, it can result in more severe metabolic dysfunction and cardiovascular outcomes later in life ( 120 ).

Other Comorbidities

Obesity is related to a clinical spectrum of liver abnormalities such as NAFLD ( 121 ); the most important cause of liver disease in children ( 122 – 124 ). NAFLD includes steatosis (increased liver fat without inflammation) and NASH (increased liver fat with inflammation and hepatic injury). While in some adults NAFLD can progress to an end-stage liver disease requiring liver transplant ( 125 , 126 ), the risk of progression during childhood is less well-defined ( 127 ). NAFLD is closely associated with metabolic syndrome including central obesity, insulin resistance, type 2 diabetes, dyslipidemia, and hypertension ( 128 ).

Obese children are also at risk for slipped capital femoral epiphysis (SCFE) ( 129 ), and sedentary lifestyle behaviors may have a negative influence on the brain structure and executive functioning, although the direction of causality is not clear ( 130 , 131 ).

Clinical Comorbidities of Obesity in Adolescents

Menstrual irregularities and pcos.

At the onset of puberty, physiologically, sex steroids can cause appropriate weight gain and body composition changes that should not affect normal menstruation ( 132 , 133 ). However, excessive weight gain in adolescent girls can result in irregular menstrual cycles and puts them at risk for PCOS due to increased androgen levels. Additionally, they can have excessive body hair (hirsutism), polycystic ovaries, and can suffer from distorted body images ( 134 , 135 ). Adolescent girls with PCOS also have an inherent risk for insulin resistance irrespective of their weight. However, weight gain further exacerbates their existing state of insulin resistance and increases the risk for obesity-related comorbidities such as metabolic syndrome, and type 2 diabetes. Although the diagnosis of PCOS can be challenging at this age due to an overlap with predictable pubertal changes, early intervention (appropriate weight loss and use of hormonal methods) can help restore menstrual cyclicity and future concerns related to childbearing ( 11 ).

Metabolic Syndrome and Sleep Disorders

Metabolic syndrome (MS) is a group of cardiovascular risk factors characterized by acanthosis nigricans, prediabetes, hypertension, dyslipidemia, and non-alcoholic steatohepatitis (NASH), that occurs from insulin resistance caused by obesity ( 136 ). Diagnosis of MS in adults requires at least three out of the five risk factors: increased central adiposity, hypertension, hyperglycemia, hypertriglyceridemia, or low HDL level. Definitions to diagnose MS are controversial in younger age groups, and many definitions have been proposed ( 136 ). This is due to the complex physiology of growth and development during puberty, which causes significant overlap between MS and features of normal growth. However, childhood obesity is associated with an inflammatory state even before puberty ( 137 ). In obese children and adolescents, hyperinsulinemia during puberty ( 138 , 139 ) and unhealthy sleep behaviors increase MS's risk and severity ( 140 ). Even though there is no consensus on diagnosis regarding MS in this age group, when dealing with obese children and adolescents, clinicians should screen them for MS risk factors and sleep behaviors and provide recommendations for weight management.

Social Psychology of Pediatric Obesity in Children and Adolescents

Obese children and adolescents may experience psychosocial sequelae, including depression, bullying, social isolation, diminished self-esteem, behavioral problems, dissatisfaction with body image, and reduced quality of life ( 13 , 141 ). Compared with normal-weight counterparts, overweight/obesity is one of the most common reasons children and adolescents are bullied at school ( 142 ). The consequence of stigma, bullying, and teasing related to childhood obesity are pervasive and can have severe implications for emotional and physical health and performance that can persist later in life ( 13 ).

In adolescents, psychological outcomes associated with obesity are multifactorial and have a bidirectional relationship ( Figure 4 ). Obese adolescents due to their physique may have a higher likelihood of psychosocial health issues, including depression, body image/dissatisfaction, lower self-esteem, peer victimization/bullying, and interpersonal relationship difficulties. They may also demonstrate reduced resilience to challenging situations compared to their non-obese/overweight counterparts ( 9 , 143 – 146 ). Body image dissatisfaction has been associated with further weight gain but can also be related to the development of a mental health disorder or an eating disorder (ED) or disorder eating habits (DEH). Mental health disorders such as depression are associated with poor eating habits, a sedentary lifestyle, and altered sleep patterns. ED or DEH that include anorexia nervosa (AN), bulimia nervosa (BN), binge-eating disorder (BED) or night eating syndrome (NES) may be related to an individual's overvaluation of their body shape and weight or can result during the treatment for obesity ( 147 – 150 ). The management of obesity can place a patient at risk of AN if there is a rigid focus on caloric intake or if a patient overcorrects and initiates obsessive self-directed dieting. Healthcare providers who primarily care for obese patients, usually give the advice to diet to lose weight and then maintain it. However, strict dieting (hypocaloric diet), which some patients may later engage in can lead to an eating disorder such as anorexia nervosa ( 151 ). This behavior leads to a poor relationship with food, and therefore, adolescents perseverate on their weight and numbers ( 152 ).

Figure 4 . Bidirectional relationship of different psychological outcomes of obesity.

Providers may not recognize DEHs when a morbidly obese patient loses the same weight as a healthy weight individual ( 149 ). It may appear as a positive result with families and others praising the individual without realizing that this youth may be engaging in destructive behaviors related to weight control. Therefore, it is essential to screen regarding the process of how weight loss was achieved ( 144 , 150 ).

Support and attention to underlying psychological concerns can positively affect treatment, overall well-being, and reduce the risk of adult obesity ( 150 ). The diagram above represents the complexity of the different psychological issues which can impact the clinical care of the obese adolescent.

Eating family meals together can improve overall dietary intake due to enhanced food choices mirrored by parents. It has also may serve as a support to individuals with DEHs if there is less attention to weight and a greater focus on appropriate, sustainable eating habits ( 148 ).

Prevention and Anticipatory Guidance

It is essential to recognize and provide preventive measures for obesity during early childhood and adolescence ( 100 , 153 , 154 ). It is well-established that early AR is a risk factor for adult obesity ( 66 – 68 ). Therefore, health care providers caring for the pediatric population need to focus on measures such as BMI but provide anticipatory guidance regarding nutritional counseling without stigmatizing or judging parents for their children's overweight/obesity ( 155 ). Although health care providers continue to pursue effective strategies to address the obesity epidemic; ironically, they frequently exhibit weight bias and stigmatizing behaviors. Research has demonstrated that the language that health care providers use when discussing a patient's body weight can reinforce stigma, reduce motivation for weight loss, and potentially cause avoidance of routine preventive care ( 155 ). In adolescents, rather than motivating positive changes, stigmatizing language regarding weight may negatively impact a teen and result in binge eating, decreased physical activity, social isolation, avoidance of health care services, and increased weight gain ( 156 , 157 ). Effective provider-patient communication using motivational interviewing techniques are useful to encourage positive behavior changes ( 155 , 158 ).

Anticipatory guidance includes educating the families on healthy eating habits and identifying unhealthy eating practices, encouraging increased activity, limiting sedentary activities such as screen time. Lifestyle behaviors in children and adolescents are influenced by many sectors of our society, including the family ( Figure 1 ) ( 3 , 24 ). Therefore, rather than treating obesity in isolation as an individual problem, it is crucial to approach this problem by focusing on the family unit. Family-based multi-component weight loss behavioral treatment is the gold standard for treating childhood obesity, and it is having been found useful in those between 2 and 6 years old ( 150 , 159 ). Additionally, empowering the parents to play an equal role in developing and implementing an intervention for weight management has shown promising results in improving the rate of obesity by decreasing screen time, promoting healthy eating, and increasing support for children's physical activity ( 160 , 161 ).

When dietary/lifestyle modifications have failed, the next option is a structured weight -management program with a multidisciplinary approach ( 15 ). The best outcomes are associated with an interdisciplinary team comprising a physician, dietician, and psychologist generally 1–2 times a week ( 15 , 162 ). However, this treatment approach is not effective in patients with severe obesity ( 122 ). Although healthier lifestyle recommendations for weight loss are the current cornerstone for obesity management, they often fail. As clinicians can attest, these behavioral and dietary changes are hard to achieve, and all too often is not effective in patients with severe obesity. Failure to maintain substantial weight loss over the long term is due to poor adherence to the prescribed lifestyle changes as well as physiological responses that resist weight loss ( 163 ). American TV hosts a reality show called “The Biggest Loser” that centers on overweight and obese contestants attempting to lose weight for a cash prize. Contestants from “The Biggest Loser” competition, had metabolic adaptation (MA) after drastic weight loss, regained more than they lost weight after 6 years due to a significant slow resting metabolic rate ( 164 ). MA is a physiological response which is a reduced basal metabolic rate seen in individuals who are losing or have lost weight. In MA, the body alters how efficient it is at turning the food eaten into energy; it is a natural defense mechanism against starvation and is a response to caloric restriction. Plasma leptin levels decrease substantially during caloric restriction, suggesting a role of this hormone in the drop of energy expenditure ( 165 ).

Pharmacological Management

The role of pharmacological therapy in the treatment of obesity in children and adolescents is limited.

Orlistat is the only FDA approved medication for weight loss in 12-18-year-olds but has unpleasant side effects ( 166 ). Another medicine, Metformin, has been used in children with signs of insulin resistance, may have some impact on weight, but is not FDA approved ( 167 ). The combination of phentermine/topiramate (Qsymia) has been FDA approved for weight loss in obese individuals 18 years and older. In studies, there has been about 9–10% weight loss over 2 years. However, caution must be taken in females as it can lead to congenital disabilities, especially with use in the first trimester of pregnancy ( 167 ).

GLP-1 agonists have demonstrated great success in effective weight loss and are approved by the FDA for adult obesity ( 168 – 170 ). A randomized control clinical trial recently published showed a significant weight loss in those using liraglutide (3.0 mg)/day plus lifestyle therapy group compared to placebo plus lifestyle therapy in children between the ages of 12–18 years ( 171 ).

Recently during the EASL conference, academic researchers and industry partners presented novel interventions targeting different gut- liver axis levels that include intestinal content, intestinal microbiome, intestinal mucosa, and peritoneal cavity ( 47 ). The focus for these therapeutic interventions within the gut-liver axis was broad and ranged anywhere from newer drugs protecting the intestinal mucus lining, restoring the intestinal barriers and improvement in the gut microbiome. One of the treatment options was Hydrogel technology which was shown to be effective toward weight loss in patients with metabolic syndrome. Hydrogel technology include fibers and high viscosity polysaccharides that absorb water in the stomach and increasing the volume, thereby improving satiety ( 47 ). Also, a clinical trial done in obese pregnant mothers using Docosahexaenoic acid (DHA) showed that the mothers' who got DHA had children with lower adiposity at 2 and 4 years of age ( 172 ). Recently the role of probiotics in combating obesity has emerged. Probiotics are shown to alter the gut microbiome that improves intestinal digestive and absorptive functions of the nutrients. Intervention including probiotics may be a possible solution to manage pediatric obesity ( 173 , 174 ). Additionally, the role of Vitamin E for treating the comorbidities of obesity such as diabetes, hyperlipidemia, NASH, and cardiovascular risk, has been recently described ( 175 , 176 ). Vitamin E is a lipid- soluble compound and contains both tocopherols and tocotrienols. Tocopherols have lipid-soluble antioxidants properties that interact with cellular lipids and protects them from oxidation damage ( 177 ). In metabolic disease, certain crucial pathways are influenced by Vitamin E and some studies have summarized the role of Vitamin E regarding the treatment of obesity, metabolic, and cardiovascular disease ( 178 ). Hence, adequate supplementation of Vitamin E as an appropriate strategy to help in the treatment of the prevention of obesity and its associated comorbidities has been suggested. Nonetheless, some clinical trials have shown contradictory results with Vitamin E supplementation ( 177 ). Although Vitamin E has been recognized as an antioxidant that protects from oxidative damage, however, a full understanding of its mechanism of action is still lacking.

Bariatric Surgery

Bariatric surgery has gained popularity since the early 2000s in the management of severe obesity. If performed earlier, there are better outcomes for reducing weight and resolving obesity-related comorbidities in adults ( 179 – 182 ). Currently, the indication for bariatric in adolescents; those who have a BMI >35 with at least one severe comorbidity (Type 2 Diabetes, severe OSA, pseudotumor cerebri or severe steatohepatitis); or BMI of 40 or more with other comorbidities (hypertension, hyperlipidemia, mild OSA, insulin resistance or glucose intolerance or impaired quality of life due to weight). Before considering bariatric surgery, these patients must have completed most of their linear growth and participated in a structured weight-loss program for 6 months ( 159 , 181 , 183 ). The American Society for Metabolic and Bariatric Surgery (AMBS) outlines the multidisciplinary approach that must be taken before a patient undergoing bariatric surgery. In addition to a qualified bariatric surgeon, the patient must have a pediatrician or provider specialized in adolescent medicine, endocrinology, gastroenterology and nutrition, registered dietician, mental health provider, and exercise specialist ( 181 ). A mental health provider is essential as those with depression due to obesity or vice versa may have persistent mental health needs even after weight loss surgery ( 184 ).

Roux-en-Y Gastric Bypass (RYGB), laparoscopic Sleeve Gastrectomy (LSG), and Gastric Banding are the options available. RYGB and LSG currently approved for children under 18 years of age ( 166 , 181 , 185 ). At present, gastric banding is not an FDA recommended procedure in the US for those under 18y/o. One study showed some improvements in BMI and severity of comorbidities but had multiple repeat surgeries and did not believe a suitable option for obese adolescents ( 186 ).

Compared to LSG, RYGB has better outcomes for excess weight loss and resolution of obesity-related comorbidities as shown in studies and clinical trials ( 183 , 184 , 187 ). Overall, LSG is a safer choice and may be advocated for more often ( 179 – 181 ). The effect on the Gut-Brain axis after Bariatric surgery is still inconclusive, especially in adolescents, as the number of procedures performed is lower than in adults. Those who underwent RYGB had increased fasting and post-prandial PYY and GLP-1, which could have contributed to the rapid weight loss ( 185 ); this effect was seen less often in patients with gastric banding ( 185 ). Another study in adult patients showed higher bile acid (BA) subtype levels and suggested a possible BA's role in the surgical weight loss response after LSG ( 188 ). Adolescents have lower surgical complication rates than their adult counterparts, hence considering bariatric surgery earlier rather than waiting until adulthood has been entertained ( 180 ). Complications after surgery include nutritional imbalance in iron, calcium, Vitamin D, and B12 and should be monitored closely ( 180 , 181 , 185 ). Although 5-year data for gastric bypass in very obese teens is promising, lifetime outcome is still unknown, and the psychosocial factors associated with adolescent adherence post-surgery are also challenging and uncertain.

Obesity in childhood and adolescence is not amenable to a single easily modified factor. Biological, cultural, and environmental factors such as readily available high-density food choices impact youth eating behaviors. Media devices and associated screen time make physical activity a less optimal choice for children and adolescents. This review serves as a reminder that the time for action is now. The need for interventions to change the obesogenic environment by instituting policies around the food industry and in the schools needs to be clarified. In clinical trials GLP-1 agonists are shown to be effective in weight loss in children but are not yet FDA approved. Discovery of therapies to modify the gut microbiota as treatment for overweigh/obesity through use of probiotics or fecal transplantation would be revolutionary. For the present, ongoing clinical research efforts in concert with pharmacotherapeutic and multidisciplinary lifestyle programs hold promise.

Author Contributions

AK, SL, and MJ contributed to the conception and design of the study. All authors contributed to the manuscript revision, read, and approved the submitted version.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Keywords: obesity, childhood, review (article), behavior, adolescent

Citation: Kansra AR, Lakkunarajah S and Jay MS (2021) Childhood and Adolescent Obesity: A Review. Front. Pediatr. 8:581461. doi: 10.3389/fped.2020.581461

Received: 08 July 2020; Accepted: 23 November 2020; Published: 12 January 2021.

Reviewed by:

Copyright © 2021 Kansra, Lakkunarajah and Jay. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Alvina R. Kansra, akansra@mcw.edu

This article is part of the Research Topic

Pediatric Obesity: From the Spectrum of Clinical-Physiology, Social-Psychology, and Translational Research

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• Published: 18 May 2023

Child and adolescent obesity

• Natalie B. Lister   ORCID: orcid.org/0000-0002-9148-8632 1 , 2 ,
• Louise A. Baur   ORCID: orcid.org/0000-0002-4521-9482 1 , 3 , 4 ,
• Janine F. Felix 5 , 6 ,
• Andrew J. Hill   ORCID: orcid.org/0000-0003-3192-0427 7 ,
• Claude Marcus   ORCID: orcid.org/0000-0003-0890-2650 8 ,
• Thomas Reinehr   ORCID: orcid.org/0000-0002-4351-1834 9 ,
• Carolyn Summerbell 10 &
• Martin Wabitsch   ORCID: orcid.org/0000-0001-6795-8430 11  

Nature Reviews Disease Primers volume  9 , Article number:  24 ( 2023 ) Cite this article

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The prevalence of child and adolescent obesity has plateaued at high levels in most high-income countries and is increasing in many low-income and middle-income countries. Obesity arises when a mix of genetic and epigenetic factors, behavioural risk patterns and broader environmental and sociocultural influences affect the two body weight regulation systems: energy homeostasis, including leptin and gastrointestinal tract signals, operating predominantly at an unconscious level, and cognitive–emotional control that is regulated by higher brain centres, operating at a conscious level. Health-related quality of life is reduced in those with obesity. Comorbidities of obesity, including type 2 diabetes mellitus, fatty liver disease and depression, are more likely in adolescents and in those with severe obesity. Treatment incorporates a respectful, stigma-free and family-based approach involving multiple components, and addresses dietary, physical activity, sedentary and sleep behaviours. In adolescents in particular, adjunctive therapies can be valuable, such as more intensive dietary therapies, pharmacotherapy and bariatric surgery. Prevention of obesity requires a whole-system approach and joined-up policy initiatives across government departments. Development and implementation of interventions to prevent paediatric obesity in children should focus on interventions that are feasible, effective and likely to reduce gaps in health inequalities.

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Introduction

The prevalence of child and adolescent obesity remains high and continues to rise in low-income and middle-income countries (LMICs) at a time when these regions are also contending with under-nutrition in its various forms 1 , 2 . In addition, during the COVID-19 pandemic, children and adolescents with obesity have been more likely to have severe COVID-19 requiring hospitalization and mechanical ventilation 3 . At the same time, the pandemic was associated with rising levels of childhood obesity in many countries. These developments are concerning, considering that recognition is also growing that paediatric obesity is associated with a range of immediate and long-term negative health outcomes, a decreased quality of life 4 , 5 , an increased presentation to health services 6 and increased economic costs to individuals and society 7 .

Body weight is regulated by a range of energy homeostatic and cognitive–emotional processes and a multifactorial interplay of complex regulatory circuits 8 . Paediatric obesity arises when multiple environmental factors — covering preconception and prenatal exposures, as well as broader changes in the food and physical activity environments — disturb these regulatory processes; these influences are now widespread in most countries 9 .

The treatment of obesity includes management of obesity-associated complications, a developmentally sensitive approach, family engagement, and support for long-term behaviour changes in diet, physical activity, sedentary behaviours and sleep 10 . New evidence highlights the role, in adolescents with more severe obesity, of bariatric surgery 11 and pharmacotherapy, particularly the potential for glucagon-like peptide 1 (GLP1) receptor agonists 12 .

Obesity prevention requires a whole-system approach, with policies across all government and community sectors systematically taking health into account, avoiding harmful health impacts and decreasing inequity. Programmatic prevention interventions operating ‘downstream’ at the level of the child and family, as well as ‘upstream’ interventions at the level of the community and broader society, are required if a step change in tackling childhood obesity is to be realized 13 , 14 .

In this Primer, we provide an overview of the epidemiology, causes, pathophysiology and consequences of child and adolescent obesity. We discuss diagnostic considerations, as well as approaches to its prevention and management. Furthermore, we summarize effects of paediatric obesity on quality of life, and open research questions.

Epidemiology

Definition and prevalence.

The World Health Organization (WHO) defines obesity as “abnormal or excessive fat accumulation that presents a risk to health” 15 . Paediatric obesity is defined epidemiologically using BMI, which is adjusted for age and sex because of the physiological changes in BMI during growth 16 . Global prevalence of paediatric obesity has risen markedly over the past four decades, initially in high-income countries (HICs), but now also in many LMICs 1 .

Despite attempts to standardize the epidemiological classification, several definitions of paediatric obesity are in use; hence, care is needed when comparing prevalence rates. The 2006 WHO Child Growth Standard, for children aged 0 to 5 years, is based on longitudinal observations of multiethnic populations of children with optimal infant feeding and child-rearing conditions 17 . The 2007 WHO Growth Reference is used for the age group 5–19 years 18 , and the 2000 US Centers for Disease Control and Prevention (CDC) Growth Charts for the age group 2–20 years 19 . The WHO and CDC definitions based on BMI-for-age charts are widely used, including in clinical practice. By contrast, the International Obesity Task Force (IOTF) definition, developed from nationally representative BMI data for the age group 2–18 years from six countries, is used exclusively for epidemiological studies 20 .

For the age group 5–19 years, between 1975 and 2016, the global prevalence of obesity (BMI >2 standard deviations (SD) above the median of the WHO growth reference) increased around eightfold to 5.6% in girls and 7.8% in boys 1 . Rates have plateaued at high levels in many HICs but have accelerated in other regions, particularly in parts of Asia. For the age group 2–4 years, between 1980 and 2015, obesity prevalence (IOTF definition, equivalent to an adult BMI of ≥30 kg/m 2 ) increased from 3.9% to 7.2% in boys and from 3.7% to 6.4% in girls 21 . Obesity prevalence is highest in Polynesia and Micronesia, the Middle East and North Africa, the Caribbean and the USA (Fig.  1 ). Variations in prevalence probably reflect different background levels of obesogenic environments, or the sum total of the physical, economic, policy, social and cultural factors that promote obesity 22 . Obesogenic environments include those with decreased active transport options, a ubiquity of food marketing directed towards children, and reduced costs and increased availability of nutrient-poor, energy-dense foods. Particularly in LMICs, the growth of urbanization, new forms of technology and global trade have led to reduced physical activity at work and leisure, a shift towards Western diets, and the expansion of transnational food and beverage companies to shape local food systems 23 .

Maps showing the proportions of children and adolescents living with overweight or obesity (part  a , boys; part b , girls) according to latest available data from the Global Obesity Observatory . Data might not be comparable between countries owing to differences in survey methodology.

The reasons for varying sex differences in prevalence in different countries are unclear but may relate to cultural variations in parental feeding practices for boys and girls and societal ideals of body size 24 . In 2016, obesity in the age group 5–19 years was more prevalent in girls than in boys in sub-Saharan Africa, Oceania and some middle-income countries in other regions, whereas it was more prevalent in boys than in girls in all HICs, and in East and South-East Asia 21 . Ethnic and racial differences in obesity prevalence within countries are often assumed to mirror variations in social deprivation and other social determinants of obesity. However, an independent effect of ethnicity even after adjustment for socioeconomic status has been documented in the UK, with Black and Asian boys in primary school having higher prevalence of obesity than white boys 25 .

Among individuals with obesity, very high BMI values have become more common in the past 15 years. The prevalence of severe obesity (BMI ≥120% of the 95th percentile (CDC definition), or ≥35 kg/m 2 at any age 26 , 27 ) has increased in many HICs, accounting for one-quarter to one-third of those with obesity 28 , 29 . Future health risks of paediatric obesity in adulthood are well documented. For example, in a data linkage prospective study in Israel with 2.3 million participants who had BMI measured at age 17 years, those with obesity (≥95th percentile BMI for age) had a much higher risk of death from coronary heart disease (HR 4.9, 95% CI 3.9–6.1), stroke (HR 2.6, 95% CI 1.7–4.1) and sudden death (HR 2.1, 95% CI 1.5–2.9) compared with those whose BMI fell between the 5th and 24th percentiles 30 .

Causes and risk factors

Early life is a critical period for childhood obesity development 9 , 31 , 32 , 33 . According to the Developmental Origins of Health and Disease framework, the early life environment may affect organ structure and function and influence health in later life 34 , 35 . Meta-analyses have shown that preconception and prenatal environmental exposures, including high maternal pre-pregnancy BMI and, to a lesser extent, gestational weight gain, as well as gestational diabetes and maternal smoking, are associated with childhood obesity, potentially through effects on the in utero environment 33 , 36 , 37 , 38 . Paternal obesity is also associated with childhood obesity 33 . Birthweight, reflecting fetal growth, is a proxy for in utero exposures. Both low and high birthweights are associated with later adiposity, with high birthweight linked to increased BMI and low birthweight to central obesity 33 , 39 .

Growth trajectories in early life are important determinants of later adiposity. Rapid weight gain in early childhood is associated with obesity in adolescence 32 . Also, later age and higher BMI at adiposity peak (the usual peak in BMI around 9 months of age), as well as earlier age at adiposity rebound (the lowest BMI reached between 4 and 7 years of age), are associated with increased adolescent and adult BMI 40 , 41 . Specific early life nutritional factors, including a lower protein content in formula food, are consistently associated with a lower risk of childhood obesity 42 , 43 . These also include longer breastfeeding duration, which is generally associated with a lower risk of childhood obesity 42 . However, some controversy exists, as these effects are affected by multiple sociodemographic confounding factors and their underlying mechanisms remain uncertain 44 . Some studies comparing higher and lower infant formula protein content have reported that the higher protein group have a greater risk of subsequent obesity, especially in early childhood 41 , 42 ; however, one study with a follow-up period until age 11 years found no significant difference in the risk of obesity, but an increased risk of overweight in the high protein group was still observed 42 , 43 , 45 . A high intake of sugar-sweetened beverages is associated with childhood obesity 33 , 46 .

Many other behavioural factors are associated with an increased risk of childhood obesity, including increased screen time, short sleep duration and poor sleep quality 33 , 47 , reductions in physical activity 48 and increased intake of energy-dense micronutrient-poor foods 49 . These have been influenced by multiple changes in the past few decades in the broader social, economic, political and physical environments, including the widespread marketing of food and beverages to children, the loss of walkable green spaces in many urban environments, the rise in motorized transport, rapid changes in the use of technology, and the move away from traditional foods to ultraprocessed foods.

Obesity prevalence is inextricably linked to relative social inequality, with data suggesting a shift in prevalence over time towards those living with socioeconomic disadvantage, and thus contributes to social inequalities. In HICs, being in lower social strata is associated with a higher risk of obesity, even in infants and young children 50 , whereas the opposite relationship occurs in middle-income countries 51 . In low-income countries, the relationship is variable, and the obesity burden seems to be across socioeconomic groups 52 , 53 .

Overall, many environmental, lifestyle, behavioural and social factors in early life are associated with childhood obesity. These factors cannot be seen in isolation but are part of a complex interplay of exposures that jointly contribute to increased obesity risk. In addition to multiple prenatal and postnatal environmental factors, genetic variants also have a role in the development of childhood obesity (see section Mechanisms/pathophysiology).

Comorbidities and complications

Childhood obesity is associated with a wide range of short-term comorbidities (Fig.  2 ). In addition, childhood obesity tracks into adolescence and adulthood and is associated with complications across the life course 32 , 41 , 54 , 55 .

Obesity in children and adolescents can be accompanied by various other pathologies. In addition, childhood obesity is associated with complications and disorders that manifest in adulthood (red box).

Increased BMI, especially in adolescence, is linked to a higher risk of many health outcomes, including metabolic disorders, such as raised fasting glucose, impaired glucose tolerance, type 2 diabetes mellitus (T2DM), metabolic syndrome and fatty liver disease 56 , 57 , 58 , 59 . Other well-recognized obesity-associated complications include coronary heart disease, asthma, obstructive sleep apnoea syndrome (itself associated with metabolic dysfunction and inflammation) 60 , orthopaedic complications and a range of mental health outcomes including depression and low self-esteem 27 , 55 , 57 , 61 , 62 , 63 .

A 2019 systematic review showed that children and adolescents with obesity are 1.4 times more likely to have prediabetes, 1.7 times more likely to have asthma, 4.4 times more likely to have high blood pressure and 26.1 times more likely to have fatty liver disease than those with a healthy weight 64 . In 2016, it was estimated that, at a global level by 2025, childhood obesity would lead to 12 million children aged 5–17 years with glucose intolerance, 4 million with T2DM, 27 million with hypertension and 38 million with fatty liver disease 65 . These high prevalence rates have implications for both paediatric and adult health services.

Mechanisms/pathophysiology

Body weight regulation.

Body weight is regulated within narrow limits by homeostatic and cognitive–emotional processes and a multifactorial interplay of hormones and messenger substances in complex regulatory circuits (Fig.  3 ). When these regulatory circuits are disturbed, an imbalance between energy intake and expenditure leads to obesity or to poor weight gain. As weight loss is much harder to achieve than weight gain in the long term due to the regulation circuits discussed below, the development of obesity is encouraged by modern living conditions, which enable underlying predispositions for obesity to become manifest 8 , 66 .

Body weight is predominantly regulated by two systems: energy homeostasis and cognitive–emotional control. Both homeostatic and non-homeostatic signals are processed in the brain, involving multiple hormone and receptor cascades 217 , 218 , 219 . This overview depicts the best-known regulatory pathways. The homeostatic system, which is mainly regulated by brain centres in the hypothalamus and brainstem, operates on an unconscious level. Both long-term signals from the energy store in adipose tissue (for example, leptin) and short-term hunger and satiety signals from the gastrointestinal tract signal the current nutrient status. During gastric distension or after the release of gastrointestinal hormones (multiple receptors are involved) and insulin, a temporary feeling of fullness is induced. The non-homeostatic or hedonic system is regulated by higher-level brain centres and operates at the conscious level. After integration in the thalamus, homeostatic signals are combined with stimuli from the environment, experiences and emotions; emotional and cognitive impulses are then induced to control food intake. Regulation of energy homeostasis in the hypothalamus involves two neuron types of the arcuate nucleus: neurons producing neuropeptide Y (NPY) and agouti-related peptide (AgRP) and neurons producing pro-opiomelanocortin (POMC). Leptin stimulates these neurons via specific leptin receptors (LEPR) inducing anabolic effects in case of decreasing leptin levels and catabolic effects in case of increasing leptin levels. Leptin inhibits the production of NPY and AgRP, whereas low leptin levels stimulate AgRP and NPY production resulting in the feeling of hunger. Leptin directly stimulates POMC production in POMC neurons. POMC is cleaved into different hormone polypeptides including α-melanocyte-stimulating hormone which in turn activates melanocortin 4 receptors (MC4R) of cells in the nucleus paraventricularis of the hypothalamus, leading to the feeling of satiety. CART, cocaine and amphetamine responsive transcript; IR, insulin receptor.

In principle, there are two main systems in the brain which regulate body weight 8 , 66 (Fig.  3 ): energy homeostasis and cognitive–emotional control. Energy homeostasis is predominantly regulated by brain centres in the hypothalamus and brainstem and operates at an unconscious level. Both long-term signals from the adipose tissue energy stores and short-term hunger and satiety signals from the gastrointestinal tract signal the current nutrient status 8 , 66 . For example, negative energy balance leading to reduced fat mass results in reduced leptin levels, a permanently reduced urge to exercise and an increased feeling of hunger. During gastric distension or after the release of gastrointestinal hormones and insulin, a temporary feeling of fullness is induced 8 , 66 . Cognitive–emotional control is regulated by higher brain centres and operates at a conscious level. Here, the homeostatic signals are combined with stimuli from the environment (sight, smell and taste of food), experiences and emotions 8 , 66 . Disorders at the level of cognitive–emotional control mechanisms include emotional eating as well as eating disorders. For example, the reward areas in the brain of people with overweight are more strongly activated by high-calorie foods than those in the brain of people with normal weight 67 . Both systems interact with each other, and the cognitive–emotional system is strongly influenced by the homeostatic control circuits.

Disturbances in the regulatory circuits of energy homeostasis can be genetically determined, can result from disease or injury to the regulatory centres involved, or can be caused by prenatal programming 8 , 66 . If the target value of body weight has been shifted, the organism tries by all means (hunger, drive) to reach the desired higher weight. These disturbed signals of the homeostatic system can have an imperative, irresistible character, so that a conscious influence on food intake is no longer effectively possible 8 , 66 . The most important disturbances of energy homeostasis are listed in Table  1 .

The leptin pathway

The peptide hormone leptin is primarily produced by fat cells. Its production depends on the amount of adipose tissue and the energy balance. A negative energy balance during fasting results in a reduction of circulating leptin levels by 50% after 24 h (ref. 68 ). In a state of weight loss, leptin production is reduced 69 . In the brain, leptin stimulates two neuron types of the arcuate nucleus in the hypothalamus via specific leptin receptors: neurons producing neuropeptide Y (NPY) and agouti-related peptide (AgRP) and neurons producing pro-opiomelanocortin (POMC). High leptin levels inhibit the production of NPY and AgRP, whereas low leptin levels stimulate AgRP and NPY production. By contrast, leptin directly stimulates POMC production in POMC neurons (Fig.  3 ). POMC is a hormone precursor that is cleaved into different hormone polypeptides by specific enzymes, such as prohormone convertase 1 (PCSK1). This releases α-melanocyte-stimulating hormone (α-MSH) which in turn activates melanocortin 4 receptors (MC4R) of cells in the nucleus paraventricularis of the hypothalamus, leading to the feeling of satiety. Rare, functionally relevant mutations in the genes for leptin and leptin receptor, POMC , PCSK1/3 or MC4R lead to extreme obesity in early childhood. These forms of obesity are potential indications for specific pharmacological treatments, for example setmelanotide 70 , 71 . MC4R mutations are the most common cause of monogenic obesity, as heterozygous mutations can be symptomatic depending on the functional impairment and with variable penetrance and expression. Other genes have been identified, in which rare heterozygous pathological variants are also associated with early onset obesity (Table  1 ).

Pathological changes in adipose tissue

Adipose tissue can be classified into two types, white and brown adipose tissue. White adipose tissue comprises unilocular fat cells and brown adipose tissue contains multilocular fat cells, which are rich in mitochondria 72 . A third type of adipocyte, beige adipocytes, within the white adipose tissue are induced by prolonged exposure to cold or adrenergic signalling, and show a brown adipocyte-like morphology 72 . White adipose tissue has a large potential to change its volume to store energy and meet the metabolic demands of the body. The storage capacity and metabolic function of adipose tissue depend on the anatomical location of the adipose tissue depot. Predominant enlargement of white adipose tissue in the visceral, intra-abdominal area (central obesity) is associated with insulin resistance and an increased risk of metabolic disease development before puberty. Accumulation of adipose tissue in the hips and flanks has no adverse effect and may be protective against metabolic syndrome. In those with obesity, adipose tissue is characterized by an increased number of adipocytes (hyperplasia), which originate from tissue-resident mesenchymal stem cells, and by enlarged adipocytes (hypertrophy) 73 . Adipocytes with a very large diameter reach the limit of the maximal oxygen diffusion distance, resulting in hypoxia, the development of an inflammatory expression profile (characterized by, for example, leptin, TNF and IL-6) and adipocyte necrosis, triggering the recruitment of leukocytes. Resident macrophages switch from the anti-inflammatory M2 phenotype to a pro-inflammatory M1 phenotype, which is associated with insulin resistance, further promoting local sterile inflammation and the development of fibrotic adipose tissue. This process limits the expandability of the adipose tissue for further storage of triglycerides. In the patient, the increase in fat mass in obesity is associated with insulin resistance and systemic low-grade inflammation characterized by elevated serum levels of C-reactive protein and pro-inflammatory cytokines. The limitation of adipose tissue expandability results in storage of triglycerides in other organs, such as the liver, muscle and pancreas 74 .

Genetics and epigenetics in the general population

Twin studies have found heritability estimates for BMI of up to 70% 75 , 76 . In contrast to rare monogenic forms of obesity, which are often caused by a single genetic defect with a large effect, the genetic background of childhood obesity in the general population is shaped by the joint effects of many common genetic variants, each of which individually makes a small contribution to the phenotype. For adult BMI, genome-wide association studies, which examine associations of millions of such variants across the genome at the same time, have identified around 1,000 genetic loci 77 . The largest genome-wide association studies in children, which include much smaller sample sizes of up to 60,000 children, have identified 25 genetic loci for childhood BMI and 18 for childhood obesity, the majority of which overlap 78 , 79 . There is also a clear overlap with genetic loci identified in adults, for example for FTO , MC4R and TMEM18 , but this overlap is not complete, some loci are specific to early life BMI, or have a relatively larger contribution in childhood 78 , 79 , 80 . These findings suggest that biological mechanisms underlying obesity in childhood are mostly similar to those in adulthood, but the relative influence of these mechanisms may differ at different phases of life.

The role of epigenetic processes in childhood and adolescent obesity has gained increasing attention. In children, several studies found associations between DNA methylation and BMI 81 , 82 , 83 , 84 , but a meta-analysis including data from >4,000 children identified only minimal associations 85 . Most studies support the hypothesis that DNA methylation changes are predominantly a consequence rather than a cause of obesity, which may explain the lower number of identified (up to 12) associations in children, in whom duration of exposure to a higher BMI is shorter than in adults, in whom associations with DNA methylation at hundreds of sites have been identified 85 , 86 , 87 . In addition to DNA methylation, some specific circulating microRNAs have been found to be associated with obesity in childhood 84 .

The field of epigenetic studies in childhood obesity is relatively young and evolving quickly. Future studies will need to focus on defining robust associations in blood as well as other tissues and on identifying cause-and-effect relationships. In addition, other omics, such as metabolomics and proteomics, are promising areas that may contribute to an improved aetiological understanding or may provide biological signatures that can be used as predictive or prognostic markers of childhood obesity and its comorbidities.

Parental obesity and childhood obesity

There is an established link between increased parental BMI and increased childhood BMI 88 , 89 . This link may be due to shared genetics, shared environment, a direct intrauterine effect of maternal BMI or a combination of these factors. In the case of shared genetics, the child inherits BMI-increasing genetic variants from one or both parents. Shared environmental factors, such as diet or lifestyle, may also contribute to an increased BMI in both parents and child. In addition, maternal obesity might create an intrauterine environment that programmes metabolic processes in the fetus, which increases the risk of childhood obesity. Some studies show larger effects of maternal than paternal BMI, indicating a potential causal intrauterine mechanism of maternal obesity, but evidence showing similar maternal and paternal effects is increasing. The data may indicate that there is only a limited direct intrauterine effect of maternal obesity on childhood obesity; rather, genetic effects inherited from the mother or father, or both, and/or shared environmental factors may contribute to childhood obesity risk 90 , 91 , 92 , 93 , 94 , 95 .

Diagnosis, screening and prevention

Diagnostic work-up.

The extent of overweight in clinical practice is estimated using BMI based on national charts 96 , 97 , 98 , 99 , 100 . Of note, the clinical classification of overweight or obesity differ depending on the BMI charts used and national recommendations; hence, local guidelines should be referred to. For example, the US CDC Growth Charts and several others use the 85th and 95th centile cut-points to denote overweight and obesity, respectively 19 . The WHO Growth Reference for children aged 5–19 years defines cut-points for overweight and obesity as a BMI-for-age greater than +1 and +2 SDs for BMI for age, respectively 18 . For children <5 years of age, overweight and obesity are defined as weight-for-height greater than +2 and +3 SDs, respectively, above the WHO Child Growth Standards median 17 . The IOTF and many countries in Europe use cut-points of 85th, 90th and 97th to define overweight, obesity and extreme obesity 26 .

BMI as an indirect measurement of body fat has some limitations; for example, pronounced muscle tissue leads to an increase in BMI, and BMI is not independent of height. In addition, people of different ethnicities may have different cut-points for obesity risk; for example, cardiometabolic risk occurs at lower BMI values in individuals with south Asian than in those with European ancestry 101 . Thus, BMI is best seen as a convenient screening tool that is supplemented by clinical assessment and investigations.

Other measures of body fat may help differentiate between fat mass and other tissues. Some of these tools are prone to low reliability, such as body impedance analyses (high day-to-day variation and dependent on level of fluid consumption) or skinfold thickness (high inter-observer variation), or are more expensive or invasive, such as MRI, CT or dual-energy X-ray absorptiometry, than simpler measures of body composition or BMI assessment.

Primary diseases rarely cause obesity in children and adolescents (<2%) 102 . However, treatable diseases should be excluded in those with obesity. A suggested diagnostic work-up is summarized in Fig.  4 . Routine measurement of thyroid-stimulating hormone (TSH) is not recommended 96 . Moderately elevated TSH levels (usually <10 IU/l) are frequently observed in obesity and are a consequence, and not a cause, of obesity 103 . In a growing child with normal height velocity, a normal BMI at the age of 2 years and normal cognitive development, no further diagnostic steps are necessary to exclude primary diseases 96 , 104 .

Concerning findings from a detailed medical history and physical examination will lead to further examinations. In individuals with early onset, extreme obesity (before age 3 years) and signs of hyperphagia, serum leptin level should be measured to rule out the extremely rare condition of congenital leptin deficiency. In individuals with normal or high leptin levels, genetic testing is indicated to search for monogenetic obesity. In individuals with intellectual disability, a syndromic disease may be present. Signs of impaired growth velocity or the history of central nervous system trauma or surgery will result in deeper endocrine evaluation and/or brain MRI. BDNF , brain-derived neurotropic factor; FT4, free thyroxin; KSR2 , kinase suppressor of ras 2; MC4R , melanocortin 4 receptor; POMC , pro-opiomelanocortin; SH2B1 , Src-homology 2 (SH2) B adapter protein 1; SIM1 , single-minded homologue 1; TSH, thyroid-stimulating hormone.

Clinical findings which need no further examination include pseudogynaecomastia (adipose tissue mimicking breast development; differentiated from breast tissue by ultrasonography), striae (caused by rapid weight increase) and a hidden penis in suprapubic adipose tissue (differentiated from micropenis by measurement of stretched penis length while pressing down on the suprapubic adipose tissue) 96 , 105 . Girls with obesity tend to have an earlier puberty onset (usually at around 8–9 years of age) and boys with severe obesity may have a delayed puberty onset (usually at around 13–14 years of age) 106 . Thus, if pubertal onset is slightly premature in girls or slightly delayed in boys, no further endocrine assessment is necessary.

Assessment of obesity-associated comorbidities

A waist to height ratio of >0.5 is a simple tool to identify central obesity 107 , 108 . Screening for cardiometabolic risk factors and fatty liver disease is recommended, especially in adolescents, and in those with more severe obesity or central adiposity, a strong family history of T2DM or premature heart disease, or relevant clinical symptoms, such as high blood pressure or acanthosis nigricans 96 , 97 , 98 , 99 , 109 . Investigations generally include fasting glucose levels, lipid profile, liver function and glycated haemoglobin, and might include an oral glucose tolerance test, polysomnography, and additional endocrine tests for polycystic ovary syndrome 96 , 97 , 98 , 99 .

T2DM in children and adolescents often occurs in the presence of a strong family history and may not be related to obesity severity 110 . T2DM onset usually occurs during puberty, a physiological state associated with increased insulin resistance 111 and, therefore, screening for T2DM should be considered in children and adolescents with obesity and at least one risk factor (family history of T2DM or features of metabolic syndrome) starting at pubertal onset 112 . As maturity-onset diabetes of the young (MODY) type II and type III are more frequent than T2DM in children and adolescents in many ethnicities, genetic screening for MODY may be appropriate 112 . Furthermore, type 1 diabetes mellitus (T1DM) should be excluded by measurement of autoantibodies in any individual with suspected diabetes with obesity. The differentiation of T2DM from MODY and T1DM is important as the diabetes treatment approaches differ 112 .

Several comorbidities of obesity should be considered if specific symptoms occur 96 , 109 . For polycystic ovary syndrome in hirsute adolescent girls with oligomenorrhoea or amenorrhoea, moderately increased testosterone levels and decreased sex hormone binding globulin levels are typical laboratory findings 113 . Obstructive sleep apnoea can occur in those with more severe obesity and who snore, have daytime somnolence or witnessed apnoeas. Diagnosis is made by polysomnography 114 . Minor orthopaedic disorders, such as flat feet and genu valgum, are frequent in children and adolescents with obesity and may cause pain. Major orthopaedic complications include slipped capital femoral epiphyses (acute and chronic), which manifest with hip and knee pain in young adolescents and are characterized by reduced range of hip rotation and waddling gait; and Blount disease (tibia vara), typically occurring in children aged 2–5 years 105 , 115 . In addition, children and adolescents with extreme obesity frequently have increased dyspnoea and decreased exercise capacity. A heightened demand for ventilation, elevated work of breathing, respiratory muscle inefficiency and diminished respiratory compliance are caused by increased truncal fat mass. This may result in a decreased functional residual capacity and expiratory reserve volume, ventilation to perfusion ratio abnormalities and hypoxaemia, especially when supine. However, conventional respiratory function tests are only mildly affected by obesity except in extreme cases 116 . Furthermore, gallstones should be suspected in the context of abdominal pain after rapid weight loss, which can be readily diagnosed via abdominal ultrasonography 105 . Finally, pseudotumor cerebri may present with chronic headache, and depression may present with flat affect, chronic fatigue and sleep problems 105 .

Obesity in adolescents can also be associated with disordered eating, eating disorders and other psychological disorders 117 , 118 . If suspected, assessment by a mental health professional is recommended.

A comprehensive approach

The 2016 report of the WHO Commission on Ending Childhood Obesity stated that progress in tackling childhood obesity has been slow and inconsistent, with obesity prevention requiring a whole-of-government approach in which policies across all sectors systematically take health into account, avoiding harmful health impacts and, therefore, improving population health and health equity 13 , 119 . The focus in developing and implementing interventions to prevent obesity in children should be on interventions that are feasible, effective and likely to reduce health inequalities 14 . Importantly, the voices of children and adolescents living with social disadvantage and those from minority groups must be heard if such interventions are to be effective and reduce inequalities 120 .

Figure  5 presents a system for the prevention of childhood obesity within different domains of the socioecological model 121 and highlights opportunities for interventions. These domains can be described on a continuum, from (most downstream) individual and interpersonal (including parents, peers and wider family) through to organizational (including health care and schools), community (including food, activity and environment), society (including media and finally cultural norms) and (most upstream) public policy (from local to national level). Interventions to prevent childhood obesity can be classified on the Nuffield intervention ladder 122 . This framework was proposed by the Nuffield Council on Bioethics in 2007 (ref. 122 ) and distributes interventions on the ladder steps depending on the degree of agency required by the individual to make the behavioural changes that are the aim of the intervention. The bottom step of the ladder includes interventions that provide information, which requires the highest agency and relies on a child, adolescent and/or family choosing (and their ability to choose) to act on that information and change behaviour. The next steps of the ladder are interventions that enable choice, guide choice through changing the default policy, guide choice through incentives, guide choice through disincentives, or restrict choice. On the top-most step of the ladder (lowest agency required) are interventions that eliminate choice.

This schematic integrates interventions that were included in a Cochrane review 127 of 153 randomized controlled trials of interventions to prevent obesity in children and are high on the Nuffield intervention ladder 122 . The Nuffield intervention ladder distributes interventions depending on the degree of agency required for the behavioural changes that are the aim of the intervention. The socioecological model 121 comprises different domains (or levels) from the individual up to public policy. Interventions targeting the individual and interpersonal domains can be described as downstream interventions, and interventions within public policy can be described as the highest level of upstream interventions. Within each of these domains, arrow symbols with colours corresponding to the Nuffield intervention ladder category are used to show interventions that were both included in the Cochrane review 127 and that guide, restrict or eliminate choice as defined by the Nuffield intervention ladder 122 . Upstream interventions, and interventions on the top steps of the Nuffield ladder, are more likely to reduce inequalities. NGO, non-governmental organization.

Downstream and high-agency interventions (on the bottom steps of the Nuffield ladder) are more likely to result in intervention-generated inequalities 123 . This has been elegantly described and evidenced, with examples from the obesity prevention literature 124 , 125 . A particularly strong example is a systematic review of 38 interventions to promote healthy eating that showed that food price (an upstream and low-agency intervention) seemed to decrease inequalities, all interventions that combined taxes and subsidies consistently decreased inequalities, and downstream high-agency interventions, especially dietary counselling, seemed to increase inequalities 126 .

Effectiveness of prevention interventions

A 2019 Cochrane review of interventions to prevent obesity in children 127 included 153 randomized controlled trials (RCTs), mainly in HICs (12% were from middle-income countries). Of these RCTs, 56% tested interventions in children aged 6–12 years, 24% in children aged 0–5 years, and 20% in adolescents aged 13–18 years. The review showed that diet-only interventions to prevent obesity in children were generally ineffective across all ages. Interventions combining diet and physical activity resulted in modest benefits in children aged 0–12 years but not in adolescents. However, physical activity-only interventions to prevent obesity were effective in school-age children (aged 5–18 years). Whether the interventions were likely to work equitably in all children was investigated in 13 RCTs. These RCTs did not indicate that the strategies increased inequalities, although most of the 13 RCTs included relatively homogeneous groups of children from disadvantaged backgrounds.

The potential for negative unintended consequences of obesity prevention interventions has received much attention 128 . The Cochrane review 127 investigated whether children were harmed by any of the strategies; for example, by having injuries, losing too much weight or developing damaging views about themselves and their weight. Of the few RCTs that did monitor these outcomes, none found any harms in participants.

Intervention levels

Most interventions (58%) of RCTs in the Cochrane review aimed to change individual lifestyle factors via education-based approaches (that is, simply provide information) 129 . In relation to the socioecological model, only 11 RCTs were set in the food and physical activity environment domain, and child care, preschools and schools were the most common targets for interventions. Of note, no RCTs were conducted in a faith-based setting 130 . Table  2 highlights examples of upstream interventions that involve more than simply providing information and their classification on the Nuffield intervention ladder.

Different settings for interventions to prevent childhood obesity, including preschools and schools, primary health care, community settings and national policy, offer different opportunities for reach and effectiveness, and a reduction in inequalities.

Preschools and schools are key settings for public policy interventions for childhood obesity prevention, and mandatory and voluntary food standards and guidance on physical education are in place in many countries. Individual schools are tasked with translating and implementing these standards and guidance for their local context. Successful implementation of a whole-school approach, such as that used in the WHO Nutrition-Friendly Schools Initiative 131 , is a key factor in the effectiveness of interventions. Careful consideration should be given to how school culture can, and needs to, be shifted by working with schools to tailor the approach and manage possible staff capacity issues, and by building relationships within and outside the school gates to enhance sustainability 132 , 133 .

Primary health care offers opportunities for guidance for obesity prevention, especially from early childhood to puberty. Parent-targeted interventions conducted by clinicians in health-care or community settings have the strongest level of evidence for their effectiveness in reducing BMI z -score at age 2 years 134 . These interventions include group programmes, clinic nurse consultations, mobile phone text support or nurse home visiting, and focusing on healthy infant feeding, healthy childhood feeding behaviours and screen time.

A prospective individual participant data meta-analysis of four RCTs involving 2,196 mother–baby dyads, and involving nurse home visiting or group programmes, resulted in a small but significant reduction in BMI in infants in the intervention groups compared with control infants at age 18–24 months 134 . Improvements were also seen in television viewing time, breastfeeding duration and feeding practices. Interventions were more effective in settings with limited provision of maternal and child health services in the community. However, effectiveness diminished by age 5 years without further intervention, highlighting the need for ongoing interventions at each life stage 135 . Evidence exists that short-duration interventions targeting sleep in very early childhood may be more effective than nutrition-targeted interventions in influencing child BMI at age 5 years 136 .

Primary care clinicians can provide anticipatory guidance, as a form of primary prevention, to older children, adolescents and their families, aiming to support healthy weight and weight-related behaviours. Clinical guidelines recommend that clinicians monitor growth regularly, and provide guidance on healthy eating patterns, physical activity, sedentary behaviours and sleep patterns 97 , 100 . Very few paediatric trials have investigated whether this opportunistic screening and advice is effective in obesity prevention 100 . A 2021 review of registered RCTs for the prevention of obesity in infancy found 29 trials 137 , of which most were delivered, or were planned to be delivered, in community health-care settings, such as nurse-led clinics. At the time of publication, 11 trials had reported child weight-related outcomes, two of which showed a small but significant beneficial effect on BMI at age 2 years, and one found significant improvements in the prevalence of obesity but not BMI. Many of the trials showed improvements in practices, such as breastfeeding and screen time.

At the community level, local public policy should be mindful of the geography of the area (such as urban or rural) and population demographics. Adolescents usually have more freedom in food and beverage choices made outside the home than younger children. In addition, physical activity levels usually decline and sedentary behaviours rise during adolescence, particularly in girls 138 , 139 . These behavioural changes offer both opportunities and barriers for those developing community interventions. On a national societal level, public policies for interventions to prevent obesity in children include the control of advertising of foods and beverages high in fat, sugar and/or salt in some countries. Industry and the media, including social media, can have a considerable influence on the food and physical activity behaviours of children 13 , 119 .

Public policy may target interventions at all domains from the individual to the societal level. The main focus of interventions in most national public policies relies on the ability of individuals to make the behavioural changes that are the aim of the intervention (high-agency interventions) at the individual level (downstream interventions). An equal focus on low-agency and upstream interventions is required if a step change in tackling childhood obesity is to be realized 140 , 141 .

COVID-19 and obesity

Early indications in several countries show rising levels of childhood obesity, and an increase in inequalities in childhood obesity during the COVID-19 pandemic 142 . The substantial disruptions in nutrition and lifestyle habits of children during and since the pandemic include social isolation and addiction to screens 143 . Under-nutrition is expected to worsen in poor countries, but obesity rates could increase in middle-income countries and HICs, especially among vulnerable groups, widening the gap in health and social inequalities 143 . Public health approaches at national, regional and local levels should include strategies that not only prevent obesity and under-nutrition, but also reduce health inequalities.

In summary, although most trials of obesity prevention have occurred at the level of the individual, the immediate family, school or community, effective prevention of obesity will require greater investment in upstream, low-agency interventions.

Treatment goals

Treatment should be centred on the individual and stigma-free (Box  1 ) and may aim for a reduction in overweight and improvement in associated comorbidities and health behaviours. Clinical considerations when determining a treatment approach should include age, severity of overweight and the presence of associated complications 144 , 145 .

Box 1 Strategies for minimizing weight stigma in health care 220 , 221 , 222

Minimizing weight bias in the education of health-care professionals

Improved education of health professionals:

pay attention to the implicit and explicit communication of social norms

include coverage of the broader determinants of obesity

include discussion of harms caused by social and cultural norms and messages concerning body weight

provide opportunities to practise non-stigmatizing care throughout education

Provide causal information focusing on the genetic and/or socioenvironmental determinants of weight.

Provide empathy-invoking interventions, emphasizing size acceptance, respect and human dignity.

Provide a weight-inclusive approach, by emphasizing that all individuals, regardless of size, have the right to equal health care.

Addressing health facility infrastructure and processes

Provide appropriately sized chairs, blood pressure cuffs, weight scales, beds, toilets, showers and gowns.

Use non-stigmatizing language in signage, descriptions of clinical services and other documentation.

Providing clinical leadership and using appropriate language within health-care settings

Senior clinicians and managers should role-model supportive and non-biased behaviours towards people with obesity and indicate that they do not tolerate weight-based discrimination in any form.

Staff should identify the language that individuals prefer in referring to obesity.

Use person-first language, for example a ‘person with obesity’ rather than ‘an obese person’.

Treatment guidelines

Clinical guidelines advise that first-line management incorporates a family-based multicomponent approach that addresses dietary, physical activity, sedentary and sleep behaviours 97 , 99 , 109 , 146 . This approach is foundational, with adjunctive therapies, especially pharmacotherapy and bariatric surgery, indicated under specific circumstances, usually in adolescents with more severe obesity 144 , 145 . Guideline recommendations vary greatly among countries and are influenced by current evidence, and functionality and resourcing of local health systems. Hence, availability and feasibility of therapies differs internationally. In usual clinical practice, interventions may have poorer outcomes than is observed in original studies or anticipated in evidence-based guidelines 147 because implementation of guidelines is more challenging in resource-constrained environments 148 . In addition, clinical trials are less likely to include patients with specialized needs, such as children from culturally diverse populations, those living with social disadvantage, children with complex health problems, and those with severe obesity 149 , 150 .

Behavioural interventions

There are marked differences in individual responses to behavioural interventions, and overall weight change outcomes are often modest. In children aged 6–11 years, a 2017 Cochrane review 150 found that mean BMI z -scores were reduced in those involved in behaviour-changing interventions compared with those receiving usual care or no treatment by only 0.06 units (37 trials; 4,019 participants; low-quality evidence) at the latest follow-up (median 10 months after the end of active intervention). In adolescents aged 12–17 years, another 2017 Cochrane review 149 found that multicomponent behavioural interventions resulted in a mean reduction in weight of 3.67 kg (20 trials; 1,993 participants) and reduction in BMI of 1.18 kg/m 2 (28 trials; 2,774 participants). These effects were maintained at the 24-month follow-up. A 2012 systematic review found significant improvements in LDL cholesterol triglycerides and blood pressure up to 1 year from baseline following lifestyle interventions in children and adolescents 151 .

Family-based behavioural interventions are recommended in national level clinical practice guidelines 97 , 100 , 146 , 152 . They are an important element of intensive health behaviour and lifestyle treatments (IHBLTs) 109 . Family-based approaches use behavioural techniques, such as goal setting, parental monitoring or modelling, taught in family sessions or in individual sessions separately to children and care givers, depending on the child’s developmental level. The priority is to encourage the whole family to engage in healthier behaviours that result in dietary improvement, greater physical activity, and less sedentariness. This includes making changes to the family food environment and requires parental monitoring.

Family-based interventions differ in philosophy and implementation from those based on family systems theory and therapy 153 . All are intensive interventions that require multiple contact hours (26 or more) with trained specialists delivered over an extended period of time (6–12 months) 10 . Changing family lifestyle habits is challenging and expensive, and the therapeutic expertise is not widely available. Moving interventions to primary care settings, delivered by trained health coaches, and supplemented by remote contact (for example by phone), will improve access and equity 154 .

Very few interventions use single psychological approaches. Most effective IHBLTs are multicomponent and intensive (many sessions), and include face-to-face contact. There has been interest in motivational interviewing as an approach to delivery 155 . As client-centred counselling, this places the young person at the centre of their behaviour change. Fundamental to motivational interviewing is the practitioner partnership that helps the young person and/or parents to explore ambivalence to change, consolidate commitment to change, and develop a plan based on their own insights and expertise. Evidence reviews generally support the view that motivational interviewing reduces BMI. Longer interventions (>4 months), those that assess and report on intervention fidelity, and those that target both diet and physical activity are most effective 155 , 156 .

More intensive dietary interventions

Some individuals benefit from more intensive interventions 98 , 144 , 157 , 158 , which include very low-energy diets, very low-carbohydrate diets and intermittent energy restriction 159 . These interventions usually aim for weight loss and are only recommended for adolescents who have reached their final height. These diets are not recommended for long periods of time due to challenges in achieving nutritional adequacy 158 , 160 , and lack of long-term safety data 158 , 161 . However, intensive dietary interventions may be considered when conventional treatment is unsuccessful, or when adolescents with comorbidities or severe obesity require rapid or substantial weight loss 98 . A 2019 systematic review of very low-energy diets in children and adolescents found a mean reduction in body weight of −5.3 kg (seven studies) at the latest follow‐up, ranging from 5 to 14.5 months from baseline 161 .

Pharmacological treatment

Until the early 2020s the only drug approved in many jurisdictions for the treatment of obesity in adolescents was orlistat, a gastrointestinal lipase inhibitor resulting in reduced uptake of lipids and, thereby, a reduced total energy intake 162 . However, the modest effect on weight in combination with gastrointestinal adverse effects limit its usefulness overall 163 .

A new generation of drugs has been developed for the treatment of both T2DM and obesity. These drugs are based on gastrointestinal peptides with effects both locally and in the central nervous system. GLP1 is an incretin that reduces appetite and slows gastric motility. The GLP1 receptor agonist liraglutide is approved for the treatment of obesity in those aged 12 years and older both in the USA and Europe 164 , 165 . Liraglutide, delivered subcutaneously daily at a higher dose than used for T2DM resulted in a 5% better BMI reduction than placebo after 12 months 166 . A 2022 trial of semaglutide, another GLP1 receptor agonist, delivered subcutaneously weekly in adolescents demonstrated 16% weight loss after 68 weeks of treatment, with modest adverse events and a low drop-out rate 12 . Tirzepatide, an agonist of both GLP1 and glucose-dependent insulinotropic polypeptide (GIP), is approved by the FDA for the treatment of T2DM in adults 167 . Subcutaneous tirzepatide weekly in adults with obesity resulted in ~20% weight loss over 72 weeks 168 . Of note, GIP alone increases appetite, but the complex receptor–agonist interaction results in downregulation of the GIP receptors 169 , illustrating why slightly modified agonists exert different effects. A study of the use of tirzepatide in adolescents with T2DM has been initiated but results are not expected before 2027 (ref. 170 ). No trials of tirzepatide are currently underway in adolescents with obesity but without T2DM.

Hypothalamic obesity is difficult to treat. Setmelanotide is a MC4R agonist that reduces weight and improves quality of life in most people with LEPR and POMC mutations 71 . In trials of setmelanotide, 8 of 10 participants with POMC deficiency and 5 of 11 with LEPR deficiency had weight loss of at least 10% at ~1 year. The mean percentage change in most hunger score from baseline was −27.1% and −43.7% in those with POMC deficiency and leptin receptor deficiency, respectively 71 .

In the near future, effective new drugs with, hopefully, an acceptable safety profile will be available that will change the way we treat and set goals for paediatric obesity treatment 171 .

Bariatric surgery

Bariatric surgery is the most potent treatment for obesity in adolescents with severe obesity. The types of surgery most frequently used are sleeve gastrectomy and gastric bypass, both of which reduce appetite 172 . Mechanisms of action are complex, involving changes in gastrointestinal hormones, neural signalling, bile acid metabolism and gut microbiota 173 . Sleeve gastrectomy is a more straightforward procedure and the need for vitamin supplementation is lower than with gastric bypass. However, long-term weight loss may be greater after gastric bypass surgery 174 .

Prospective long-term studies demonstrate beneficial effects of both sleeve gastrectomy and gastric bypass on weight loss and comorbidities in adolescents with severe obesity 175 , 176 . In a 5-year follow-up period, in 161 participants in the US TEEN-LABS study who underwent gastric bypass, mean BMI declined from 50 to 37 kg/m 2 (ref. 11 ). In a Swedish prospective study in 81 adolescents who underwent gastric bypass, the mean decrease in BMI at 5 years was 13.1 kg/m 2 (baseline BMI 45.5 kg/m 2 ) compared with a BMI increase of 3.1 kg/m 2 in the control group 176 . Both studies showed marked inter-individual variations. Negative adverse effects, including gastrointestinal problems, vitamin deficits and reduction in lean body mass, are similar in adults and adolescents. Most surgical complications following bariatric surgery in the paediatric population are minor, occurring in the early postoperative time frame, but 8% of patients may have major perioperative complications 177 . Up to one-quarter of patients may require subsequent related procedures within 5 years 109 . However, many adolescents with severe obesity also have social and psychological problems, highlighting the need for routine and long-term monitoring 109 , 178 .

Recommendations for bariatric surgery in adolescents differ considerably among countries, with information on long-term outcomes emerging rapidly. In many countries, bariatric surgery is recommended only from Tanner pubertal stage 3–4 and beyond, and only in children with severe obesity and cardiometabolic comorbidities 177 . The 2023 American Academy of Pediatrics clinical practice guidelines recommend that bariatric surgery be considered in adolescents ≥13 years of age with a BMI of ≥35 kg/m 2 or 120% of the 95th percentile for age and sex, whichever is lower, as well as clinically significant disease, such as T2DM, non-alcoholic fatty liver disease, major orthopaedic complications, obstructive sleep apnoea, the presence of cardiometabolic risk, or depressed quality of life 109 . For those with a BMI of ≥40 kg/m 2 or 140% of the 95th percentile for age and sex, bariatric surgery is indicated regardless of the presence of comorbidities. Potential contraindications to surgery include correctable causes of obesity, pregnancy and ongoing substance use disorder. The guidelines comment that further evaluation, undertaken by multidisciplinary centres that offer bariatric surgery for adolescents, should determine the capacity of the patient and family to understand the risks and benefits of surgery and to adhere to the required lifestyle changes before and after surgery.

Long-term weight outcomes

Few paediatric studies have investigated long-term weight maintenance after the initial, more intensive, weight loss phase. A 2018 systematic review of 11 studies in children and adolescents showed that a diverse range of maintenance interventions, including support via face-to-face psychobehavioural therapies, individual physician consultations, or adjunctive therapeutic contact via newsletters, mobile phone text or e-mail, led to stabilization of BMI z -score compared with control participants, who had increases in BMI z -score 179 . Interventions that are web-based or use mobile devices may be particularly useful in young people 180 .

One concern is weight regain which occurs after bariatric surgery in general 181 but may be more prevalent in adolescents 176 . For example, in a Swedish prospective study, after 5 years, 25–30% of participants fulfilled the definitions of low surgical treatment effectiveness, which was associated with poorer metabolic outcomes 176 . As with adults, prevention of weight regain for most at-risk individuals might be possible with the combination of lifestyle support and pharmacological treatment 182 . Further weight maintenance strategies and long-term outcomes are discussed in the 2023 American Academy of Pediatrics clinical practice guidelines 109 . The appropriate role and timing of other therapies for long-term weight loss maintenance, such as anti-obesity medications, more intensive dietary interventions and bariatric surgery, are areas for future research.

In summary, management of obesity in childhood and adolescence requires intensive interventions. Emerging pharmacological therapies demonstrate greater short-term effectiveness than behavioural interventions; however, long-term outcomes at ≥2 years remain an important area for future research.

Quality of life

Weight bias describes the negative attitudes to, beliefs about and behaviour towards people with obesity 183 . It can lead to stigma causing exclusion, and discrimination in work, school and health care, and contributes to the inequities common in people with obesity 184 . Weight bias also affects social engagement and psychological well-being of children.

Children and adolescents with obesity score lower overall on health-related quality of life (HRQoL) 4 , 5 . In measures that assess domains of functioning, most score lower in physical functioning, physical/general health and psychosocial areas, such as appearance, and social acceptance and functioning. HRQoL is lowest in treatment-seeking children and in those with more extreme obesity 185 . Weight loss interventions generally increase HRQoL independent of the extent of weight loss 186 , especially in the domains most affected. However, changes in weight and HRQoL are often not strongly correlated. This may reflect a lag in the physical and/or psychosocial benefit from weight change, or the extent of change that is needed to drive change in a child’s self-perception.

Similar observations apply to the literature on self-esteem. Global self-worth is reduced in children and adolescents with obesity, as is satisfaction with physical appearance, athletic competence and social acceptance 187 . Data from intensive interventions suggest the psychological benefit of weight loss may be as dependent on some feature of the treatment environment or supportive social network as the weight loss itself 188 . This may include the daily company of others with obesity, making new friendships, and experienced improvements in newly prioritized competences.

There is a bidirectional relationship between HRQoL and obesity 189 , something also accepted in the relationship with mood disorder. Obesity increases the risk of depression and vice versa, albeit over a longer period of time and which may only become apparent in adulthood 190 . Obesity also presents an increased risk of anxiety 191 .

Structured and professionally delivered weight management interventions ameliorate mood disorder symptoms 192 and improve self-esteem 193 . Regular and extended support are important components beyond losing weight. Such interventions do not increase the risk of eating disorders 194 . This is despite a recognition that binge eating disorder is present in up to 5% of adolescents with overweight or obesity 195 . They are five times more likely to have binge eating symptoms than those with average weight. Importantly, adolescents who do not have access to professionally delivered weight management may be more likely to engage in self-directed dieting, which is implicated in eating disorder development 196 .

The literature linking childhood obesity with either attention deficit hyperactivity disorder or autism spectrum disorder is complex and the relationship is uncertain. The association seems to be clearer in adults but the mechanisms and their causal directions remain unclear 109 , 197 . Young children with obesity, especially boys, are more likely to be parent-rated as having behavioural problems 198 . This may be a response to the behaviour of others rather than reflect clinical diagnoses such as attention deficit hyperactivity disorder or autism spectrum disorder. Conduct and peer relationship problems co-occur in children, regardless of their weight.

Children with obesity experience more social rejection. They receive fewer friendship nominations and more peer rejections, most pronounced in those with severe obesity 199 . This continues through adolescence and beyond. Children with obesity are more likely to report being victimized 200 . Younger children may respond by being perpetrators themselves. While it is assumed that children are victimized because of their weight, very few studies have looked at the nature or reason behind victimization. A substantial proportion of children with obesity fail to identify themselves as being fat-teased 187 . Although the stigma associated with obesity should be anticipated in children, especially in those most overweight, it would be inappropriate to see all as victims. A better understanding of children’s resilience is needed.

Many gaps remain in basic, translational and clinical research in child and adolescent obesity. The mechanisms (genetic, epigenetic, environmental and social) behind the overwhelming association between parental obesity and child and adolescent obesity are still unclear given the paradoxically weak association in BMI between adopted children and their parents in combination with the modest effect size of known genetic loci associated with obesity 201 .

Early manifestation of extreme obesity in childhood suggests a strong biological basis for disturbances of homeostatic weight regulation. Deep genotyping (including next-generation sequencing) and epigenetic analyses in these patients will reveal new genetic causes and causal pathways as a basis for the development of mechanism-based treatments. Future work aiming to understand the mechanisms underlying the development of childhood obesity should consider the complex biopsychosocial interactions and take a systems approach to understanding causal pathways leading to childhood obesity to contribute to evidence-based prevention and treatment strategies.

Long-term outcome data to better determine the risks of eating disorders are required. Although symptoms improve during obesity treatment in most adolescents, screening and monitoring for disordered eating is recommended in those presenting for treatment 202 and effective tools for use in clinical practice are required. A limited number of tools are validated to identify binge eating disorder in youth with obesity 203 but further research is needed to screen appropriately for the full spectrum of eating disorder diagnoses in obesity treatment seeking youth 203 . Recent reviews provide additional detail regarding eating disorder risk in child and adolescent obesity 117 , 202 , 204 .

Most studies of paediatric obesity treatment have been undertaken in HICs and predominantly middle-class populations. However, research is needed to determine which strategies are best suited for those in LMICs and low-resource settings, for priority population groups including indigenous peoples, migrant populations and those living with social disadvantage, and for children with neurobehavioural and psychiatric disorders. We currently have a limited understanding of how best to target treatment pathways for different levels of genetic risk, age, developmental level, obesity severity, and cardiometabolic and psychological risk. Current outcomes for behavioural interventions are relatively modest and improved treatment outcomes are needed to address the potentially severe long-term health outcomes of paediatric obesity. Studies also need to include longer follow-up periods after an intervention, record all adverse events, incorporate cost-effectiveness analyses and have improved process evaluation.

Other areas in need of research include the role of new anti-obesity medications especially in adolescents, long-term outcomes following bariatric surgery and implementation of digital support systems to optimize outcomes and reduce costs of behavioural change interventions 205 . We must also better understand and tackle the barriers to implementation of treatment in real-life clinical settings, including the role of training of health professionals. Importantly, treatment studies of all kinds must engage people with lived experience — adolescents, parents and families — to understand what outcomes and elements of treatment are most valued.

Obesity prevention is challenging because it requires a multilevel, multisectoral approach that addresses inequity, involves many stakeholders and addresses both the upstream and the downstream factors influencing obesity risk. Some evidence exists of effectiveness of prevention interventions operating at the level of the child, family and school, but the very poor progress overall in modifying obesity prevalence globally highlights many areas in need of research and evidence implementation. Studies are needed especially in LMICs, particularly in the context of the nutrition transition and the double burden of malnutrition. A focus on intergenerational research, rather than the age-based focus of current work, is also needed. Systems research approaches should be used, addressing the broader food and physical activity environments, and links to climate change 206 . In all studies, strategies are needed that enable co-production with relevant communities, long-term follow-up, process evaluation and cost-effectiveness analyses. In the next few years, research and practice priorities must include a focus on intervention strategies in the earliest phases of life, including during pregnancy. The effects of COVID-19 and cost of living crises in many countries are leading to widening health inequalities 207 and this will further challenge obesity prevention interventions. Available resourcing for prevention interventions may become further constrained, requiring innovative solutions across agendas, with clear identification of co-benefits. For example, public health interventions for other diseases, such as dental caries or depression, or other societal concerns, such as urban congestion or climate change, may also act as obesity prevention strategies. Ultimately, to implement obesity prevention, societal changes are needed in terms of urban planning, social structures and health-care access.

Future high-quality paediatric obesity research can be enabled through strategies that support data sharing, which avoids research waste and bias, and enables new research questions to be addressed. Such approaches require leadership, careful engagement of multiple research teams, and resourcing. Four national or regional level paediatric weight registries exist 208 , 209 , 210 , 211 , which are all based in North America or Europe. Such registries should be established in other countries, especially in low-resource settings, even if challenging 208 . Another data-sharing approach is through individual participant data meta-analyses of intervention trials, which can include prospectively collected data 212 and are quite distinct from systematic reviews of aggregate data. Two recent examples are the Transforming Obesity Prevention in Childhood (TOPCHILD) Collaboration, which includes early interventions to prevent obesity in the first 2 years of life 213 , and the Eating Disorders in Weight-Related Therapy (EDIT) Collaboration, which aims to identify characteristics of individuals or trials that increase or protect against eating disorder risk following obesity treatment 214 . Formal data linkage studies, especially those joining up routine administrative datasets, enable longer-term and broader outcome measures to be assessed than is possible with standard clinical or public health intervention studies.

Collaborative research will also be enhanced through the use of agreed core outcome sets, supporting data harmonization. The Edmonton Obesity Staging System – Paediatric 215 is one option for paediatric obesity treatment. A core outcome set for early intervention trials to prevent obesity in childhood (COS-EPOCH) has been recently established 216 . These efforts incorporate a balance between wanting and needing to share data and adhering to privacy protection regulations. Objective end points are ideal, including directly measured physical activity and body composition.

Collaborative efforts and a systems approach are paramount to understand, prevent and manage child and adolescent obesity. Research funding and health policies should focus on feasible, effective and equitable interventions.

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Introduction (L.A.B., J.F.F. and N.B.L.); Epidemiology (L.A.B. and J.F.F.); Mechanisms/pathophysiology (L.A.B., J.F.F., T.R. and M.W.); Diagnosis, screening and prevention (L.A.B., N.B.L., T.R., C.S. and M.W.); Management (L.A.B., N.B.L., A.J.H., C.M. and T.R.); Quality of life (L.A.B., N.B.L. and A.J.H.); Outlook (L.A.B., N.B.L., J.F.F., A.J.H., C.M., T.R., C.S. and M.W.); Overview of the Primer (L.A.B. and N.B.L.).

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A.J.H. reports receiving payment for consultancy advice for Slimming World (UK). L.A.B. reports receiving honoraria for speaking in forums organized by Novo Nordisk in relation to management of adolescent obesity and the ACTION-Teens study, which is sponsored by Novo Nordisk. L.A.B. is the Australian lead of the study. T.R. received funding from the German Federal Ministry of Education and Research (BMBF; 01GI1120A/B) as part of the German Competence Network Obesity (Consortium ‘Youth with Extreme Obesity’). T.R. receives payment for consultancy advice related to pharmacological treatment of obesity from Novo Nordisk and Lilly, as well as honoraria for lectures in symposia organized by Novo Nordisk, Novartis and Merck. C.M. receives payments for consultancy advice and advisory board participation from Novo Nordisk, Oriflame Wellness, DeFaire AB and Itrim AB. C.M. also receives honoraria for speaking at meetings organized by Novo Nordisk and Astra Zeneca. C.M. is a shareholder and founder of Evira AB, a company that develops and sells systems for digital support for weight loss, and receives grants from Novo Nordisk for epidemiological studies of the effects of weight loss on future heath. M.W. received funding from the German Federal Ministry of Education and Research (BMBF; 01GI1120A/B) as part of the German Competence Network Obesity (Consortium ‘Youth with Extreme Obesity’). M.W. receives payment for consultancy advice related to pharmacological treatment of obesity from Novo Nordisk, Regeneron, Boehringer Ingelheim and LG Chem, as well as honoraria for speaking in symposia organized by Novo Nordisk, Rhythm Pharmaceuticals and Infectopharm. M.W. is principal investigator in phase II and phase III studies of setmelanotide sponsored by Rhythm Pharmaceuticals. N.B.L., J.F.F. and C.S. declare no competing interests.

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Lister, N.B., Baur, L.A., Felix, J.F. et al. Child and adolescent obesity. Nat Rev Dis Primers 9 , 24 (2023). https://doi.org/10.1038/s41572-023-00435-4

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Nutritional Management in Childhood Obesity

1 Research Institute of Medical Nutrition, Kyung Hee University, Seoul, Korea

Hyunjung Lim

2 Department of Medical Nutrition, Graduate School of East-West Medical Science, Kyung Hee University, Yongin, Korea

The increasing prevalence of overweight and obese children and adolescents poses a major concern worldwide. Dietary practice in these critical periods affects physical and cognitive development and has consequences in later life. Therefore, acquiring healthy eating behaviors that will endure is important for children and adolescents. Nutrition management has been applied to numerous childhood obesity intervention studies. Diverse forms of nutrition education and counseling, key messages, a Mediterranean-style hypocaloric diet, and nutritional food selection have been implemented as dietary interventions. The modification of dietary risk in terms of nutrients, foods, dietary patterns, and dietary behaviors has been applied to changing problematic dietary factors. However, it is not easy to identify the effectiveness of nutritional management because of the complex and interacting components of any multicomponent approach to intervention in childhood obesity. In this review, we describe the modifiable dietary risk factors and nutritional components of previous nutrition intervention studies for nutritional management in childhood obesity. Furthermore, we suggest evidence-based practice in nutrition care for obese children and adolescents by considering obesity-related individual and environmental dietary risk factors.

INTRODUCTION

The childhood obesity epidemic has reached 124 million individuals, and nearly one in five children and adolescents are overweight or obese. 1 The worldwide trend in childhood obesity shows a steadily increasing body mass index (BMI) in children and adolescents across four decades. In East and South Asia, including South Korea, the BMI increase among children and adolescents has accelerated since 2000. 2 The prevalence of obesity in children and adolescents increased from 11.6% in 2008 to 17.3% in 2017. 3 Obesity in early life is of concern due to health consequences and its influence on later life. 4 Increased adiposity levels are strongly associated with developing metabolic disorders and signs of adverse cardiometabolic diseases. 5 The severity of these comorbidities typically increases with the severity of the obesity. 6

Dietary- and health-related behaviors and food preferences are established in early childhood and continue into adulthood. 7 Poor food choices and overconsumption are associated with a higher risk of developing obesity. 8 The prevalence of diet-related metabolic disorders such as obesity, glucose intolerance, elevated blood pressure, and dyslipidemia is increasing due to unbalanced food intake among adolescents. 9 Dietary factors are the most important factors associated with childhood obesity, 10 and prevalence rates of nutrition-related noncommunicable diseases such as obesity and diabetes in children and adolescents have prompted prioritizing healthy diets. 1

Dietary intervention and multisectoral approach intervention studies have reported positive changes in body composition and dietary factors for overweight and obese children and adolescents. 11 – 16 Dietary components such as energy-dense foods, sugar-sweetened beverages (SSBs) and patterns of processed food consumption are discussed among the modifiable risk factors associated with obesity in children and adolescents. 17 – 19 In the present review, we describe the dietary risk factors associated with childhood obesity and summarize the previous efforts at nutrition management in multisectoral interventions. In addition, we suggest customized nutrition care for obese children and adolescents to improve young children’s dietary factors.

DIETARY RISK FACTORS IN CHILDHOOD OBESITY

Numerous diet-related modifiable risk factors (nutrients, foods, dietary patterns, and eating behaviors) have been considered in previous clinical research studies and suggested in guidelines on childhood obesity ( Table 1 ). A higher intake of saturated fats and carbohydrates, including the overconsumption of energy-dense foods such as pizza, soda, and SSBs, has been associated with obesity in children and adolescents. 20 , 21 Dietary patterns during childhood have identified associations between diet and diseases such as diabetes, hypertension, cardiometabolic risk, and childhood obesity. 4 , 18 , 22 The Western dietary pattern, which contains high amounts of saturated fatty acids, is energy-dense, is micronutrient poor, and is limited in non-starch polysaccharides (fiber), is known to be a dietary risk factor encouraging childhood obesity. 17 , 23 Diet patterns that are rich in meat, soda, fried food, instant noodles, burgers, and pizza increased the risk of obesity by 30% compared to diet patterns rich in whole grains, legumes, potatoes, fish, mushrooms, seaweed, fruits, and vegetables. 24

Diet-related modifiable factors affecting childhood obesity

Guidelines and recommendations 17 – 19 , 23 , 24 , 26 – 34 , 36 – 40 of diet-related modifiable factors for nutritional management in childhood obesity.

Unhealthy eating habits and patterns formed during childhood have been associated with nutrition-related noncommunicable diseases such as obesity and diabetes. 25 Sedentary behavior among children and adolescents, higher intake of snacks, consumption of SSBs, fast food consumption, eating while watching television, skipping breakfast, reduced numbers of family meal times spent eating together, and lower daily intake of milk, fruits, and vegetables have all been associated with increased rates of childhood obesity, leading to adverse health and dietary outcomes. 26 , 27

Meanwhile, an adequate nutritional intake of vitamins and minerals, whole grains, milk and dairy products, fruits, and vegetables in a balanced diet has been found to not only protect growth but also manage childhood obesity. 17 , 28 – 31 In addition, it is recommended that proper dietary behaviors with family support include meals at home, eating together as a family, regular mealtimes, and portion sizes appropriate for the daily requirements of children and adolescents. 19 , 32 , 33

NUTRITION-BASED MULTIDISCIPLINARY INTERVENTION COMPONENTS AFFECTING CHILDHOOD OBESITY

Systematic reviews have suggested that multiple strategies and components and a multilevel approach that focuses on diet and health-related activities have provided the most sustainable and beneficial effects on childhood obesity intervention, rather than single-component interventions. 34 , 35 Furthermore, social support such as individualized coaching, text messaging, face-to-face communication, and Internet-based approaches with a theoretical background have been adapted to change obesity-related dietary behaviors in children and adolescents. 12 – 16 , 41 – 43 The most promising approaches for childhood obesity management are intervening with support at levels ranging from individual to community via sustainable and multisectoral strategies. 44

Let’s Move was a program of the U.S. government in collaboration with the American Academy of Pediatrics intended to provide Internet-based resources for BMI and diet and to develop activity screening in primary care, including counseling and advocacy methods for healthcare professionals. 11 Consistent with this initiative, innovative use of health information technology was implemented via individualized coaching for behavior change, 12 text messaging to provide outreach support for obesity management, 41 and study-specific website and email programs, which had achievements similar to those found with face-to-face support. 42

The B’More Healthy Communities for Kids trial was a multilevel childhood obesity prevention intervention guided by social cognitive theory, social ecology, and systems theory. According to these theories, psychosocial factors, social-environmental factors, and physical factors interact at multiple levels to shape health-related outcomes. 13 In this study, wholesalers, corner stores, take-out restaurants, recreation centers, and households worked together to improve availability, purchasing, and consumption of healthier foods and beverages (low sugar, low fat) in low-income African American zones in the city of Baltimore, MD, USA. 13

The Childhood Obesity Demonstration (CORD) project was designed to cover 4 years, including three grantees, Massachusetts (MA CORD), California (CA CORD), and Texas (TX CORD), funded by the Centers for Disease Control and Prevention. 14 This set of three unique multilevel, multi-setting demonstration projects aimed to prevent childhood obesity by supporting healthy eating and active living among 2- to 12-year-old children. The results from the MA CORD study included changes in organizational policies and environments to better support healthy living and improvements in health behaviors of children, parents, and stakeholders. 15

The identification and prevention of dietary- and lifestyle-induced health effects in children and infants (IDEFICS) study was developed by eight European countries to implement and evaluate diet- and lifestyle-related diseases and was strongly focused on childhood obesity in a large population-based cohort of 16,228 European children aged 2 to 9 years. 16 The IDEFICS intervention focused on the three main concepts of nutrition, physical activity, and stress, and it formulated six key messages. The prospective study reported that children consistently allocated to the “processed” cluster increased their BMI, waist circumference, and fat mass gain compared to children allocated to the “healthy” cluster. Being in the “processed”–“sweet” cluster combination was also linked to increased BMI, waist circumference, and fat mass gain over time compared to the “healthy” cluster. 43

RECENT DIETARY INTERVENTIONS AND OUTCOMES

We performed a systematic review of the literature for identifying the effectiveness of nutritional interventions using the electronic databases PubMed, Cochrane Library, and Web of Science, covering the past 5 years (2015 through August 2019). The following search terms were used: childhood obesity, obese children and adolescents, nutritional intervention, and dietary outcomes. Trials published in English were included in this study; the primary outcomes examined were energy, nutrient intake, fruit and vegetable consumption, and dietary behaviors.

Dietary interventions

Only articles on dietary outcomes were extracted from the databases by two researchers. Six studies 45 – 50 are summarized in Table 2 among the dietary intervention studies that were selected by titles and abstracts. Nutritional components (nutrition education, key messages, Mediterranean-style hypocaloric diet, and nutritional food selection) and outcomes (energy and nutrient intake; fruit, vegetable, and dairy product consumption; and dietary behaviors) of the dietary intervention studies are presented in Table 2 .

Changes in dietary factors and weight status of children and adolescents after participating in nutritional interventions

PA: physical activity; BMI, body mass index; CAFAP: Curtin University’s Activity, Food and Attitudes Program.

Nutrition education was delivered by health instructors at selected schools. Face-to-face training was used, with a book for guidance when necessary, for weekly nutrition sessions for the participants. Monthly lifestyle education sessions focusing on childhood obesity and its causes, cooking methods, and plans to reduce inactivity were provided to parents of the participants. 45 Curtin University’s Activity, Food and Attitudes Program (CAFAP) study focused on healthy food choices and key messages: eat more fruit; eat more vegetables; and eat less junk food. Regarding general nutritional themes, energy balance, food labeling, diet variety, fast food, lunchbox food, portion size, and recipe modification were the key topics reinforced in each session, delivered in 12 group education sessions with parents and adolescents together. Parents took part in nutritional sessions and in practical training in shopping at a supermarket and cooking classes for healthy foods such as fruits and vegetables. 46

The Intervention Grupo Navarro de Estudio de la Obe- sidad Infantil study consisted of an 8-week phase and a 2-year follow-up program. The usual care group received standard pediatric recommendations and anthropometric measurements, while the intensive care group was advised to adhere to a Mediterranean-style hypocaloric diet. Nutritional theme-based topics included controlling healthy lifestyle behavior, food preparation, portion control, eating behavior, food composition, and the importance of being physically active during leisure time. In addition, information on healthy lifestyles and how to manage obesity-related problems was provided to the caregivers by dietitians. 48

The Nereu Program (NP) was an intensive, 8-month, family-based, multicomponent behavioral intervention on healthy eating and physical activity in 6- to 12-year-old children who were overweight and obese. The NP consisted of the following four components: physical activity, family theoretical and practical training for parents, a behavioral component for both children and parents, and activities. For the usual treatment group, a 10-minute monthly family meeting based on the same NP components was provided over an 8-month period. Based on the food frequency questionnaire and main nutritional characteristics, the intervention addressed the following foods for participants and their families: all fruits, which have high levels of antioxidants, fiber, and vitamins; processed meats, which contain fatty acids; superfluous foods characterized by a high level of lipid content and/or simple sugars; and soft drinks, which have a high simple sugar content without nutrients. 49

The school-based Educació en Alimentació (the EdAl study) 50 program was designed to verify the sustainability of the benefits from a previous EdAl study by assessing the obesity-related outcomes and lifestyles of 13- to 15-year-old adolescents. The EdAl program was comprised of 12 educational intervention activities that were based on improving health-related habits such as nutritional food selection, hand washing, and avoiding sedentary behavior. 50

Energy and nutrient intake

Two studies reported higher energy, protein, and fat intake after the intervention compared to baseline. 45 , 46 Despite the lack of positive changes in macronutrient intake, lower levels of saturated fat and sugar consumption were presented in the CAFAP cohort study. In another multidisciplinary intervention study, lower energy intake and macronutrient intake were reported after the dietary intervention (at 8 weeks) in both the usual care group and the intensive care group. 47

Consumption of fruits, vegetables, and dairy products

Improvements in consumption of fruits and vegetables among the children and adolescents were reported in three of the multicomponent-approach intervention studies. 46 – 49 Smith et al. 46 stated that perceived fruit consumption and vegetable consumption of the participants were higher after the dietary intervention. Ojeda-Rodríguez et al. 47 and Serra-Paya et al. 49 presented higher levels of dairy product consumption as well as fruit and vegetable consumption after the intervention in both groups. Meanwhile, a 4-year follow-up study showed decreased consumption of dairy products, fruits, and fish among children and adolescents. 50

Unhealthy dietary behaviors

Lower consumption levels of sugar-sweetened juices and soft drinks and sweet, superfluous foods (cookies, pastries, dairy-based desserts, and French fries, which contain high levels of lipids and/or simple sugars) were shown after the dietary intervention in three of the preceding studies. 46 , 47 , 49

Body composition

Most of the studies showed decreased BMI z-scores of obese children and adolescents after 6 weeks to 6 months for each of the intervention studies. Theme-based nutritional sessions, involving portion size and food groups, 51 feelings of hunger and satisfaction, 52 nutrition counseling and phone calls, 53 nutrition education group sessions and leaflets for caregivers, 54 healthful and balanced diet with fruits and vegetables, 55 and healthy beverage intake and increased consumption of fruits, nuts, legumes, vegetables, fish, and dairy products 50 were implemented in childhood obesity intervention studies (data not shown).

EFFECTS OF INDIVIDUALIZED NUTRITIONAL MANAGEMENT ON CHILDHOOD OBESITY

There are numerous risk factors for obesity in children and adolescents, and these factors interact with a high level of complexity. The nutritional care process model (NCP) 56 ( Fig. 1 ) could be adapted well to this complex task through dietitian-delivered lifestyle interventions. 57 The Academy of Nutrition and Dietetics developed the NCP, a highly qualified systematic approach to care, by employing four interrelated steps: nutritional assessment, diagnosis, intervention, and monitoring/evaluation. There is a requirement for standardizing the NCP and increasing the quality and consistency of nutritional care by using the International Dietetics and Nutrition Terminology (IDNT). 58 , 59 Previously, we developed a study protocol 60 to manage the dietary problems of moderately to severely obese children and adolescents by adopting the NCP and IDNT. Three general domains—nutrition intake, nutrition clinical, and nutritional behavioral—were employed for nutritional diagnosis ( Table 3 ). Nutrition diagnosis is the act of identifying a disease or condition from its signs and symptoms by a dietetics profession. An identified nutritional problem is summarized into a structured sentence called a PES (Problem, Etiology, Symptom) statement. This statement is linked by the connecting terms problem/nutrition diagnosis related to etiology as evidenced by the signs and symptoms. The identified etiology, signs and symptoms point to a certain type of nutrition intervention and monitoring/evaluation that is needed. It is an important process in the implementation of a nutrition intervention and monitoring/evaluation of the NCP. A structured recommendation for nutritional management of childhood obesity was presented as a tool in another research study that helped practitioners structure their actions according to the four interrelated steps of the NCP model. This practice-based, evidence-informed approach assisted not only the dietitians but also the professionals in pediatric obesity. The NCP four-step structured framework made it possible to structure patient-centered nutritional care and management of childhood obesity. 61

Nutrition Care Process and Model. Academy of Nutrition and Dietetics. Adapted from Lacey and Pritchett. J Am Diet Assoc 2003;103:1061–72, with permission from Elsevier. 56

Adoptable nutrition diagnosis of NCP components employed while using IDNT for childhood obesity

NCP, nutritional care process model; IDNT, International Dietetics and Nutrition Terminology; DRI, dietary reference intake; FBG, fasting blood glucose; BMI, body mass index.

Dietary intervention with a multisectoral approach has had positive outcomes in modifying obesity-related dietary risk factors for obese children and adolescents. Excellent results from previous meta-analyses have reported a reduction in SSB intake and changes in body fatness, 62 reduction in high-fat food and sugary beverages, increased intake of fruits and vegetables, reduction in snacks, and maintenance of a balanced diet. 63

These positive changes were found immediately after the intervention; however, unfavorable outcomes were reported after long-term follow-up in terms of weight fluctuation, increased energy intake, macronutrient intake, and unhealthy dietary behaviors. Furthermore, it is hard to distinguish isolated impacts of nutrition care in childhood obesity because of the complex and interacting components of the multidisciplinary interventions. 64 Behavioral modification and motivational interviewing on the health and diet of children and adolescents, to improve their self-control and mindful eating for sustainable healthy weight and nutritional status, are required to provide nutritional education and management.

From this viewpoint, evidence-based practice in dietary problem solving can suggest effective methods by considering behavioral and environmental risk factors in a diet and providing tailored nutritional therapy according to the stages of change among children and adolescents. In spite of these beneficial effects, we are facing barriers to providing this intervention due to the time and cost of developing more methods for countering childhood obesity. For this reason, individual, familial, social, and political-level involvement are recommended for effective and sustainable nutritional management of childhood obesity. In addition, practical key messages for health and diet may be helpful in establishing healthful habits and lifestyles in this public health crisis.

ACKNOWLEDGMENTS

We thank Seran Choi and Nayoung Kim from Kyung Hee University for assisting with the review and identifying recent intervention studies.

CONFLICTS OF INTEREST

The authors declare no conflict of interest.

AUTHOR CONTRIBUTIONS

Study concept and design: HL; analysis and interpretation of data: JK; drafting of the manuscript: all authors; critical revision of the manuscript: all authors; administrative, technical, or material support: JK; and study supervision: HL.