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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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Obesity effects on child health.

Palanikumar Balasundaram ; Sunil Krishna .

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Last Update: April 10, 2023 .

• Continuing Education Activity

Obesity in childhood is the most challenging public health issue in the twenty-first century. Childhood obesity is associated with increased morbidity and premature death. Prevention of obesity in children is a high priority in the current situation. This activity reviews the etiology, pathophysiology, and consequence of childhood obesity and also highlights the role of the interprofessional team in the prevention and management of childhood obesity.

• Outline the definition of childhood obesity.
• Describe the etiology and pathophysiology of childhood obesity.
• Summarize the consequences of childhood obesity.
• Explain how interprofessional teamwork can improve effective management interventions for childhood obesity.
• Introduction

Obesity in childhood is the most challenging public health issue in the twenty-first century. It has emerged as a pandemic health problem worldwide. The children who are obese tend to stay obese in adulthood and prone to increased risk for diabetes and cardiac problems at a younger age. Childhood obesity is associated with increased morbidity and premature death. [1] Prevention of obesity in children is a high priority in the current situation.

Epidemiology

The prevalence of childhood obesity has alarmingly increased. The overall burden of obesity has almost tripled since 1975. However, an eightfold increase in obesity burden in the 5 to 19 years age group has been noted between 1975 and 2016. [2] Though childhood obesity is more prevalent in developed countries, the prevalence is increasing even in developing countries. [3] Currently, about 18.5% of US children present with obesity. Among boys, obesity is more prevalent in the school-age group (6 to 11 years), whereas in girls, it is more prevalent in adolescents (12 to 19 years). The prevalence of childhood obesity among boys and girls was not significantly different overall or by age groups. [4]

The word obesity infers the deposition of excessive fat in the body. Different methods can directly measure body fat like skinfold thickness, hydro densitometry, bioelectrical impedance, and air displacement plethysmography. [5] These methods are not readily available in the clinical setting and are expensive. Body mass index (BMI) provides an economical method to assess body fat indirectly. BMI is measured using a formula [BMI = weight (kg)/ height (m)^2]. [6] [7] As growth in children varies with age and sex, so do the norms for BMI. The following definitions are used to classify weight status based on BMI for children from 2 to 20 years of age. [8] [9]

• Overweight – 85th to less than the 95th percentile.
• Obese (class 1) – 95th percentile or greater
• Severe (class II) obesity – ≥ 120% of 95th percentile (99th percentile) or ≥ 35 kg/m^2 (whichever is lower)
• Class III obesity is a subcategory of severe obesity and is defined as BMI ≥140 % of 95th percentile or ≥ 40 kg/m^2. 

The World Health Organization (WHO) recommends using BMI Z-score cut-offs of >1, > 2, and > 3 to define at risk of overweight, overweight, and obesity, respectively. [7] Z-score is measured in terms of standard deviations from the mean.

• Issues of Concern

Etiology and Pathophysiology

The complex interaction of individual and environmental factors plays a crucial role in developing obesity. The most important factors contributing to childhood obesity are summarized below. 

Environmental Factors

Changes in the environment in the past few decades in terms of easy access/ affordability of high-calorie fast food, increased portion size, increased intake of sugary beverages, and sedentary lifestyles are associated with increased incidence of obesity. [10] Increasing use of electronic devices [television, tablets, smartphone, videogames] by children has led to limited physical activity, disruption of the sleep-wake cycle, depression of metabolic rate, and poor eating patterns. [11]

Feeding patterns in infancy have a long-term effect on developing obesity later on in life. It has been shown that breastfeeding in the first year of life is inversely associated with weight gain and obesity. [12] This association was much more significant if the child was exclusively breastfed compared to having added formula or solid food. Despite concerns about the risk for obesity in preterm and SGA infants receiving calorie and protein supplementation, it has been shown to improve catch-up growth without increasing the risk of obesity. [13] High protein intake in the initial two years of life has also been postulated to increase weight gain later in childhood. 

Biological Factors

There is a complex interaction between the neural, hormonal, and gut-brain axis affecting hunger and satiety. Hypothalamus regulates appetite and is influenced by key hormones, ghrelin, and leptin. Ghrelin is released from the stomach and stimulates hunger (orexigenic), whereas leptin is mainly secreted from adipose tissue and suppresses appetite (anorexigenic). Several other hormones like neuropeptide Y and agouti-related peptide stimulate hunger, while pro-melanocortin and α-melanocyte-stimulating hormone suppress hunger. [14] These hormones control energy balance by stimulating the hunger and satiety centers in the arcuate nucleus of the hypothalamus through various signaling pathways. Stress-related psychiatric disorders with associated abnormal sleep-wake cycles can also lead to increased ghrelin levels and, in turn, increase appetite.

The gut microbiome includes the trillions of microorganisms that inhabit the human gut. Alterations in the gut microbiome can lead to weight gain through numerous pathways. [15] The dominant gut florae are Firmicutes and Bacteroidetes (90%), Proteobacteria , Actinobacteria , and Fusobacteria . These bacteria have a symbiotic relationship with their host. They can be affected by various factors, such as gestational age at birth, premature rupture of membranes, mode of delivery of the infant, type of feeding, feeding practices, and antibiotics usage. The maturation of gut flora occurs from birth to adulthood and is determined by various genetic factors, diet, lifestyle, and environment. Gut microbiota helps maintain the mucosal barrier, nutrient digestion (especially the synthesis of short-chain fatty acids), and immune response against pathogens. The imbalance of the gut microbiome (dysbiosis), leading to increased production of short-chain fatty acids, has been linked to developing obesity and other medical conditions, such as type 2 Diabetes Mellitus, Metabolic syndrome, anxiety, and depression. [16]

Genetic Factors

Obesity can be either monogenic, syndromic, or polygenic types. Monogenic obesity is uncommon, occurring in 3% to 5% of obese children. [17] Mutations in genes for leptin, leptin receptor, proopiomelanocortin, and melanocortin-4 receptor can lead to obesity. Monogenic type presents in early childhood with unusual feeding behaviors and severe obesity.

Genetic syndromes causing severe obesity include

• Prader Willi syndrome:  Early growth faltering followed by hyperphagia and increased weight gain by 2 to 3 years. The mild or moderate cognitive deficit, microcephaly, short stature, hypotonia, almond-shaped eyes, high-arched palate, narrow hands/feet, delayed puberty are common features.
• Alstrom syndrome:  Blindness, deafness, acanthosis nigricans, chronic nephropathy, type 2 diabetes, cirrhosis, primary hypogonadism in males, and normal cognition are common features in Alstrom syndrome.
• Bardet Biedl syndrome: Intellectual disability, hypotonia, retinitis pigmentosa, polydactyly, hypogonadism, glucose intolerance, deafness, and renal disease are the features in Bardet Biedl syndrome.
• Other syndromes include Beckwith-Weideman syndrome and Cohen syndrome.

Polygenic obesity is much more common and is caused by a complex interaction between multiple genetic variants and the environment known as gene-environment interaction (GEI). When a child with genotype variants conferring risk for obesity interacts with various environmental factors predisposing to obesity, there is a tendency for decreased physical activity, increased food intake, and body fat storage. Early life environment starting with maternal nutrition during the prenatal or early postnatal period and early childhood adverse environmental or psychosocial stressors can lead to epigenetic changes leading to obesity.

Endocrine Factors

Endocrine causes constitute less than 1% of cases of obesity in children. [18] It is usually associated with mild to moderate obesity, short stature, or hypogonadism. These include cortisol excess [steroid medications or Cushing syndrome], hypothyroidism, growth hormone deficiency, and pseudohypoparathyroidism.

Medications

Numerous medications can cause weight gain. These include antiepileptics, antidepressants, antipsychotics, diabetes medications [insulin, sulfonylureas, thiazolidinediones], glucocorticoids, progestins, antihistamines [cyproheptadine], alpha-blockers [terazosin], and beta-blockers [propranolol]. Close monitoring for excessive weight gain should be done when any of these medications are used in children.

Endocrine-disrupting chemicals, such as bisphenol A and dichlorodiphenyltrichloroethane, have been hypothesized to predispose to obesity by modulating estrogen receptors and possibly metabolic programming. [19]

Few studies in animal models have proven that obesity can be triggered by infection with adenovirus. However, human studies have found conflicting results.

• Clinical Significance

Childhood obesity significantly impacts both physical and psychological health. Obesity can lead to severe health conditions, including non-insulin-dependent diabetes, cardiovascular problems, bronchial asthma, obstructive sleep apnea (OSA), hypertension, hepatic steatosis, gastroesophageal reflux (GER), and psychosocial issues. The preventive and therapeutic interventions in childhood obesity are crucial in decreasing the burden of comorbid health conditions.

Metabolic Syndrome

Metabolic syndrome, also named syndrome X, is a cluster of risk factors specific for cardiovascular diseases such as hypertension, glucose intolerance, dyslipidemia, and abdominal obesity that commonly occur in obese children or adolescents. Insulin resistance, hyperinsulinemia, and oxidative stress are the underlying factors contributing to metabolic syndrome. [20]  

Dyslipidemia

Atherogenic dyslipidemia is common in obese children and adolescents. A fasting lipoprotein level needs to be obtained in all children with obesity. Elevated triglycerides (TG) and Free fatty acid (FFA) levels, decreased HDL (high-density lipoprotein) cholesterol levels, and normal or mildly increased serum LDL (low-density lipoprotein) cholesterol levels are common findings in childhood obesity. [21] Hyperinsulinemia and insulin resistance in childhood obesity promotes hepatic delivery of FFA for triglyceride synthesis and sequestration into TG-rich lipoproteins. [22]  

Glucose Intolerance

Childhood obesity quadruples the risk of developing glucose intolerance and non-insulin-dependent diabetes mellitus (NIDDM or Type 2 diabetes). Over 85% of children with NIDDM are either overweight or obese at diagnosis. [23] Acanthosis nigricans is an increased pigmentation and thickness of the skin in intertriginous folds, and it is usually associated with glucose intolerance in children and adolescents. Fasting insulin and glucose should be included in the evaluation of childhood obesity. The risk factors for type 2 non-insulin-dependent diabetes and metabolic syndrome include, 

• children with BMI 85th to 95th percentile along with,
• immediate family history of type 2 diabetes 
• signs of insulin resistance such as acanthosis nigricans, dyslipidemia, hypertension, and polycystic ovarian syndrome.
• Children with BMI >95th percentile regardless of family history or associated features. [24]  

Hypertension

The most significant risk factor for pediatric hypertension is the high body mass index. One-fourth of obese children can have hypertension. Adipocyte is not only a storage depot for fat but is also an active endocrinological cell. The pro-inflammatory adipokines (leptin, resistin, and IL-6) lead to an increase in sympathetic nervous system (SNS) activation, which preferentially impacts the renal vascular beds. [25] Hypertension risk in childhood obesity can also be explained due to hyperinsulinemia. Hyperinsulinemia causes hypertension through secondary mechanisms such as increased renal sodium retention, increased intracellular free calcium, and increased SNS activity. [26] Dietary therapy, along with exercise, effectively decreases blood pressure. 

Hepatic Steatosis  

Pediatric liver disease is a severe complication of childhood obesity. Obesity-related non-alcoholic fatty liver disease (NAFLD) spectrum includes fatty liver, steatohepatitis, cirrhosis, and hepatocellular carcinoma. [27] Hyperinsulinemia in childhood obesity plays a significant role in contributing to hepatic steatosis. Gradual weight loss with regular exercise and diet with less refined carbohydrates and low-fat help normalize hepatic enzymes and resolve hepatic steatosis. [28]   

Cholelithiasis

The prevalence of cholelithiasis is high among adolescents with obesity, and the association is more robust in girls than in boys. Increased cholesterol synthesis and cholesterol saturation of bile contribute to cholelithiasis among adolescents with obesity. [29] [29]  Cholelithiasis occurs even more frequently with weight reduction. Almost half of the cases of cholecystitis in adolescents may be associated with obesity. 

Overweight or obese children have been observed to have a higher prevalence of asthma and asthma exacerbations. The link between asthma and obesity is mediated through abnormal inflammatory and oxidant stress, chest restriction with airway narrowing, and obesity-related comorbidities such as obstructive sleep apnea and gastroesophageal reflux. [30]  

Idiopathic Intracranial Hypertension 

Idiopathic intracranial hypertension (IIH) is an uncommon disease of childhood and adolescence characterized by increased intracranial pressure without any identifiable cause. Almost half of the children who present with this syndrome may be obese and also have more IIH symptoms at onset. [31]  The disease is characterized by elevated intracranial pressure. IIH presents with headaches and may lead to severe visual impairment or blindness. The potential for visual impairment indicates the need for aggressive treatment of obesity in patients with IIH.

Sleep Apnea

Obesity and overweight are crucial risk factors for obstructive sleep apnea (OSA). Neurocognitive deficits and excessive daytime sleepiness are common among obese children with sleep apnea. [32] Obesity hypoventilation syndrome may represent a long-term consequence of sleep apnea and is associated with a high mortality rate. Aggressive therapy is warranted for obese children with this syndrome. Obesity management such as increased physical activity and a healthy diet are recommended for OSA treatment, as well as surgical procedures, if appropriate. 

Orthopedic Complications

Fractures, musculoskeletal discomfort, and lower extremity malalignment such as Blount disease and slipped capital femoral epiphyses are more common in overweight than non-overweight children and adolescents. [33]  Blount disease is a disorder of the proximal tibial growth plate, which results in progressive bowing of the tibia. Although the prevalence of Blount disease is low, approximately two-thirds of Blount disease patients may be obese. Slipped capital femoral epiphysis occurs due to epiphyseal plate disruption. Between 30% and 50% of patients with slipped capital femoral epiphysis are overweight.  

Polycystic Ovary Disease 

Obesity is frequently associated with polycystic ovary disease (PCOD). Up to 30% of women with PCOD may be obese. Hyperandrogenism and hyperinsulinemia often accompany PCOD. Obesity increases the risk of PCOD through insulin resistance and compensatory hyperinsulinemia, which increases androgen production and decreases sex hormone-binding globulin, thereby increasing the bioavailability of androgen. Adolescents with PCOD are at increased risk for metabolic syndrome and glucose intolerance. Weight loss represents an important therapeutic target in obese adolescents with PCOD.  

Persistence of obesity into adulthood

About 15% to 30% of adults with obesity were also obese in their childhood or adolescence. [34]  The cardiovascular risk factors present in obese children or adolescents usually persist into adulthood. The change in body fat in obese adolescents can be a reasonable mediator contributing to the excess morbidity and mortality in later adulthood. 

Psychosocial impact 

Children with obesity or overweight are more likely to experience low self-esteem and depression during adolescence. Negative psychological experiences trigger emotional eating, leading to an ongoing obesity-depression cycle. Children who are overweight or obese face bullying at school and are excluded from competitive physical activities. Overall, children with obesity have less social interaction and spend more time in sedentary activities. Numerous studies have confirmed the association of childhood obesity with ADHD and anxiety disorders. [35]

Eating Disorders

Children with overweight or obesity have a high prevalence of disordered eating behaviors, increasing the risk of developing eating disorders. The majority of adolescents with restrictive eating disorders report a history of obesity in the past. Binge eating increases the risk of obesity and type 2 diabetes. [36]  Appropriate evaluation for eating disorders should be performed during the treatment planning of childhood obesity. 

Academic Performance 

Children who are obese and have comorbid health problems like diabetes, asthma, or sleep apnea miss school more frequently, thereby affecting their school performance negatively.

• Enhancing Healthcare Team Outcomes

Prevention is the best intervention to decrease the prevalence of obesity. The pediatrician should explore the risk of obesity and overweight during every clinical visit for all children.  

• Both bottle-fed and breastfed infants are at risk of overfeeding. However, overfeeding is more prevalent among bottle-fed infants. Exclusive breastfeeding and delayed initiation of solid foods may reduce the future risk of overweight. 
• Skim milk is a safe replacement for whole milk after two years of age. Parents or caretakers should never use food like sweets for a reward. The entire family should have a balanced diet that comprises less than 30 percent of calories from fat. AAP recommends consuming a variety of vegetables and fruits, whole grains, proteins, low-fat dairies and decreasing the intake of sodium, saturated fats, and refined sugars beginning at the age of two years. [37]
• An essential step in preventing obesity is reducing sedentary time. Limit the screen time, including television, video games, or mobile, not more than 2 hours per day for more than six-year-old children and not more than 1 hour per day for 2-6 years of age group. AAP strongly recommends not allowing kids less than two years to have screen time. [38]
• Encourage physical activity for children. Children aged 3 to 5 years should be active throughout the day. Children and adolescents ages 6 to 17 years should be physically active for at least 60 minutes every day. [39]
• As per CDC, 60% of middle school kids and 70% of high school kids do not meet the standard sleep recommendations. AAP recommends that children aged 1 to 2 years sleep 11 to 14 hours per day, children 3 to 5 years sleep 10 to 13 hours, children 6 to 12 years sleep 9 to 12 hours, and adolescents aged 13 to 18 years should regularly sleep 8 to 10 hours. [40]  Avoiding heavy meals close to bedtime, being physically active throughout the day, and removing electronic devices in the bedroom will help to get better sleep.  

The pediatrician should explore for associated morbidity in all obese children. The detailed assessment in obese children should include assessing cardiac comorbidities, orthopedic complications, and psycho-social complications.

• Reasonable weight-loss goals should be initially 5 to 10 pounds (2 kg to 4.5 kg) or a rate of 1 to 4 pounds (0.5 to 2 kg) per month.
• Dietary management:  Dieticians provide dietary prescriptions mentioning the total calories per day and recommended percentage of calories from carbohydrates, protein, and fat. The Traffic Light Plan is one method of providing dietary management. The Traffic Light Plan classifies foods as green (low energy density), yellow (moderate energy density), and red (high energy density). These categories help children in adopting healthier eating patterns.[41] The dietician plays a significant role in guiding the diet plan for the patients.
• Physical activity:  As per the fitness level, begin the physical activity with the goal of 30 minutes/day in addition to any school activity. Treatment should target gradually increasing the activity to 60 minutes per day. An exercise physiologist, along with the physician, can help the patients to achieve their target physical activity.
• Behavior modification:  Primary care-based behavioral interventions such as self-monitoring, nutritional education, improvement of eating habits, increasing physical activity, attitude change, and rewards help manage childhood obesity.
• Family involvement:  Review overall family activity and television viewing patterns and always involve parents in nutrition counseling. Family-based behavioral treatment is the most robust intervention for childhood obesity. [41]
• Psychotherapy:   Behavioral therapy and Cognitive therapy are commonly used by the psychologist in the management of obesity. Behavioral therapy trains patients to act differently around food, and cognitive therapy trains patients how to change their thoughts and emotions related to food.
• None of the anorexiant medications are FDA approved for use in childhood obesity. Orlistat is the only FDA-approved medication for use in adolescents. 
• Surgical procedures like gastric bypass have not been studied sufficiently in children to advise their use. 

An interprofessional team that provides a holistic and integrated approach can help achieve the best possible outcomes. Collaboration, shared decision making, and communication are key elements for a good outcome. Multidisciplinary teams include a primary physician, a dietician, a nurse or nurse practitioner, a clinical exercise physiologist, and a psychologist. The interprofessional team can provide a comprehensive weight loss program that benefits the patients.

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Disclosure: Sunil Krishna declares no relevant financial relationships with ineligible companies.

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• Open access
• Published: 12 June 2023

Embracing parenting role in childhood obesity

• Jiying Ling 1 &
• Mekdes Gebremariam 2  

BMC Public Health volume  23 , Article number:  1118 ( 2023 ) Cite this article

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Active parental engagement is crucial in controlling childhood obesity. However, optimal strategies to engage parents and mechanisms linking parents’ involvement to childhood obesity prevention need further investigation. In this editorial, we provide a background to invite contributions to the BMC Public Health collection titled ‘Parenting role in childhood obesity’.

Childhood obesity represents a significant global public health challenge. The prevalence of obesity has doubled in more than 70 countries since 1980; in many other countries it has continued increasing [ 1 ]. The World Health Organization’s recent estimates suggest that 1 in 5 children and adolescents are overweight or obese [ 2 ]. What is even more concerning is the disproportionate number of children with a lower socioeconomic position that are affected by this pandemic in many settings [ 3 ], contributing to health inequities. Adverse impacts of childhood obesity are wide ranging, encompassing social, economic, and health-related consequences. The latter can be both short- and long-term, and include psychosocial, neurological, dental, cardiovascular, respiratory as well as endocrine complications and comorbidities [ 4 ]. Body weight is also known to track moderately from childhood into adulthood, making early interventions particularly important.

Obesity at all ages is multifactorial and complex. Multiple models aimed at classifying the potential influences on childhood obesity have been developed. One such model is the social ecological model, a widely used model that recognizes the interplay between factors at the individual (e.g., sociodemographic characteristics, genetic predisposition, knowledge, attitude), interpersonal (e.g., role of family, friends and other social networks), community (e.g., schools, neighborhoods), societal (e.g. cultural norms, media), and public policy levels as they influence health and health behaviors [ 4 ]. Interventions aimed at promoting healthy behaviors and preventing obesity should ideally consider this complex interplay of factors. More recently, the need to acknowledge the complexity of the linkages, interactions, and feedback loops among and between these different levels, using a systems approach, has been increasingly promoted [ 5 ]. In addition, it has been suggested that adequate participation of stakeholders at different levels (e.g., children themselves, parents in family, schools) and cross-sectoral collaborations are among the factors facilitating the success of interventions in this area.

Parents serve as critical role models to shape children’s healthy lifestyle behaviors including eating behavior, physical activity, sleep, and screen time. Parental poor feeding practices, indulgent parenting style, parental stress, and unsupportive home environment are identified as home and parental characteristics contributing to childhood obesity [ 6 ]. The influence of parents on childhood obesity starts from preconception and across the entire childhood to even early adulthood. Current recommendations are calling for aggressive early childhood family-centered obesity interventions [ 7 ]. Family is the ecosystem system fostering the growth and development of children while being bounded by social determinants of health (e.g., economic stability, built environment, social context, food accessibility). When developing childhood obesity interventions, family should be the active and core partner for decision-making.

Overall, family-based interventions consisting of training, education, and practices are more effective than children-only interventions, and medium-to-strong intensity of parental involvement results in greater short- and long-term effects on controlling childhood obesity [ 8 ]. Active parental involvement is especially significant during maintenance phase to achieve long-term sustained effects. Some evidence even indicates the need to omit children from interventions to be cost-effective, because parents-only interventions have achieved equal or even greater effects on reducing overweight or obesity than targeting both children and parents [ 9 ]. Understanding how families as a system organize and manage lifestyle behaviors can help to tailor an intervention to meet family needs.

Although the positive effects of active parental engagement in controlling childhood obesity are established, optimal strategies to engage parents and the additional effects of parents’ active involvement in obesity prevention and intervention are unknown, especially among adolescents. The constant evolving technology (e.g., internet, mobile phone, social media) provides a promising avenue for actively engaging parents particularly hard-to-reach families in intervention research. However, parental participation usually fades over time along with intervention effects, but acceptability of mobile health interventions among parents are high. Moreover, future intervention efforts should focus on assessing parents’ adherence to interventions, examining the beneficial effects on parents’ outcomes, and exploring the associations between parents’ and children’s outcomes. According to the Family System Theory, family members simultaneously affect and are affected by each other, and the overall family dynamics (i.e., family functioning, family cohesion, interpersonal communication) are more powerful than the dynamics between two individual members [ 10 ]. Grounded in the Family System Theory, family-based interventions need to consider two types of changes: (1) behavioral changes of members at the family level; and (2) dynamic changes on family structure, rules, communication, and responsiveness.

In summary, parents’ role in the prevention of childhood obesity is critical and widely acknowledged. Prevention of childhood obesity however remains highly challenging with intervention effects that are often modest at best and poorly sustained over time. Adequate prevention efforts would require comprehensive intervention approaches targeting the different levels of the social ecological model. Within such approaches, the active involvement of parents and families remains crucial. More research is in this regard needed to explore the mechanisms through which parental involvement can contribute to positive environmental and behavioral changes. Optimal ways to involve parents in childhood obesity prevention efforts also need to be assessed further.

The aim of this collection is thus to contribute to the complex field of childhood obesity prevention through the publication of studies focusing on the priority areas highlighted in this editorial. We invite authors to submit studies with strong theoretical underpinning and making use of recent advances in statistics to explore causal mechanisms linking parental role and the family environment with childhood obesity. Intervention studies demonstrating how best to actively involve parents in childhood obesity prevention efforts are encouraged. We also welcome studies quantifying the impact of parental/family/home-based interventions on changes in behaviors and body weight, but also assessing mediators of such changes (e.g., family social environment), as there is a lack of obesity intervention studies reporting on the latter changes.

Data availability

Not applicable.

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Michigan State University College of Nursing, 1355 Bogue Street C241, East Lansing, Michigan, 48824, US

Jiying Ling

Department of Community Medicine, Global Health, University of Oslo Institute of Health and Society, Oslo, Norway

Mekdes Gebremariam

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Both authors contributed equally to this editorial and share first authorship. Both authors read and approved the final manuscript.

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Drs. Jiying Ling and Mekdes Gebremariam are Guest Editors of the Collection “Parenting Role in Childhood Obesity” and editorial board members of BMC Public Health.

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Ling, J., Gebremariam, M. Embracing parenting role in childhood obesity. BMC Public Health 23 , 1118 (2023). https://doi.org/10.1186/s12889-023-16039-2

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Home — Essay Samples — Nursing & Health — Childhood Obesity — Child Obesity Essay Outline

Child Obesity Essay Outline

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Reducing Childhood Obesity Essay

It is evident that childhood obesity has emerged as one of the growing global pandemics in healthcare sector. It is against this reason that empirical studies on childhood obesity have been intensified alongside enacting policies and strategies on how to curb this anomaly and encourage healthy living. Furthermore, numerous recommendations have been implemented based on the findings obtained from research studies in order to identify effective strategies that can be put in place to eradicate child obesity. Urgent actions have been taken by national decision makers in most states. However, it is imperative to note that these efforts have been faced by several challenges. For instance, from the previous reviews, it is evident that several environmental strategies have been used in response to diminishing child obesity irrespective of the challenges. Extensive research has also provided people with a criterion on the possible causes and means of eradicating child obesity. In this case, this paper aims at reviewing the external and internal validity of the research carried out on reduction of child obesity.

Meyers (2009) confirms the claim that child obesity has increasingly become prevalent among children aged between 6 and11 years. According to research evidences, it is apparent that the pediatric complications associated with obesity prolongs from childhood to adulthood. A valid evidence derived form the research indicates that there are health indicators that accompany children who are obese. Such health indicators include blood pressure, increased linear growth, hepatic problems and aged bones. Statistics have shown that 20% of children in USA are susceptible to obesity. Furthermore, it is explicit that child obesity has become a global pandemic. This document aim to support the research obtained on child obesity giving a concise and acceptable validity thus evaluate its scientific merit.

According to Krebs et al (2007), it is evident that child obesity is caused by poor dietary intake. The authors confirm that feeding children with food rich in fats and calories has been a major contributing factor towards childhood obesity. Moreover, there are other factors such as lack of enough exercise, genetic susceptibility and illnesses that are equally worrying as far as obesity is concerned. Research done on how to reduce child obesity has been supported by Sherry (2005). From the research conducted, the main objective was to identify effective means in which child obesity can be reduced. Sherry (2005) adds that some of the proposed solutions include proper exercise and taking appropriate diet. She also asserts that parents should be intensely engaged in teaching and finding out the type of diet given to their children.

From the past research done, Burns and Grove (2009) concur that innovations have been proposed to reduce infant morbidity and mortality. One of the evidence based practice (EBP) identified is education. In this case, Burns and Grove (2009) support the idea that pregnant mother should be educated on the possible signs and symptoms of obesity. Krebs et al (2007) confirms the allegation and insists that the symposiums should start at the prenatal and pre-term labor stages. Additionally, Meyers (2009) suggests that the proposed evidence-based practice (EBP) innovation will eventually ensure that parents are fully informed about the signs and symptoms of obesity. In line with this, adequate information gained will help them to seek guidance and medications incase they identify that their children are susceptible to obesity. Other than educating pregnant mothers, reports have shown that doctors and health practitioners should take the initiative and establish programs that will advocate for the need of exercises and good dietary. In this case, role of health care providers have been perceived as a form of evidence based practice to eradicate child obesity (Burns & Grove, 2009). Another evidenced based practice includes proper dietary and exercise among children. However, it is the role of the parent to advise their children on how best to go about it rather than leaving then to decide for themselves. Krebs et al (2007) emphasize on the essence of physical exercise in reducing obesity. That’s not withstanding, educating teachers has also been perceived as evidence based practice. In this case, the teacher will help children to take balanced diet and have exercise at school and homes. Finally, it is recommendable that physical facilities for exercise should be availed in schools and homes in order to ensure that children have adequate exercise daily (Mayer, 2009).

Sufficient Research Support Base

Meyer (2009) reiterates that most past researches on the proposed solutions on how to decimate child obesity were very limited with most conducted in the late 1980’s and 1990’s. Researchers, in their current research study reports cited these past study reports concerning focal topics as implementing education programs for pregnant women and home uterine monitoring (Burns & Grove, 2009). However, there is no current research studies to date that have been conducted or published concerning this much-needed evaluation-type of research and the development of workable and viable strategies, which have confirmed to reduce the morbidity and mortality rate of infants. Research done indicates that, unless the problem of child obesity is checked, the rate will increase tremendously all over the world. Anon (2007) supports this claim as he acknowledges that quite a big number of children have increasingly been exposed to the various risks associated with obesity. Sherry (2007) identifies such risks as orthopedic problems, hypertension, depression, respiratory complications and obesity. This claim has been seconded by Anon (2007) who asserts that 80% of United States children alone have one or two of the perceived risks.

Compelling Research Support Base

Throughout the research, three studies were identified and considered as relevant to the innovation described above. The studies included two quantitative and one qualitative as it is indicated in the appendix section below. The external validity of the research on reduction of child obesity was based on the fact that both qualitative and quantitative data were obtained. This increased the clarity and accuracy of the findings. Moreover, internal validity was achieved by the fact that the research was based on the right target group. In this case, target population included healthy women who obtain care from private practitioners. Moreover, Convenience sample obtained from obstetric practices.

From the findings derived in this theoretical research study, it is evident that there is a relatively high level of heterogeneity when compared to other researches conducted in the past (Burns & Grove, 2009). However, the research was prone to certain limitations including unreliable response toward the established questions. However, the research based evidences were obtained through a collaborative effort from the target group and clinical experts. For this reason, it is clear from the review that best responses were derived from the research and any form of possible bias was equally clarified.

Anon. (2007). Effective dietary interventions for overweight and obese children, Australian Nursing Journal , 14(11): 31-4.

Burns, N., & Grove, S.K. (2009). The practice of nursing research: Appraisal, synthesis, and generation of evidence . St. Louis: Saunders Elsevier.

Krebs, N. et al. (2007). Assessment of Child and Adolescent Overweight and Obesity. Pediatrics: Supplement , 120, S193.

Mayer, K. (2009). Childhood Obesity Prevention: Focusing on the Community Food Environment . Family and Community Health , 32(3): 257.

Sherry, B. (2005). Food behaviors and other strategies to prevent and treat pediatric overweight. International Journal of Obesity , 29(S2), S116-26.

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