Strategies for Prevention of Childhood Obesity

C H A P T E R

24 Strategies for Prevention of Childhood Obesity Satinath Mukhopadhyay*, Sunetra Mondal*, and Sudip Chatterjee†

*Department of Endocrinology & Metabolism, Institute of Post Graduate Medical Education & Research (IPGMER) and SSKM Hospital, Kolkata, India † Department of Endocrinology, Vivekananda Institute of Medical Sciences, Kolkata, India, and Park Clinic, Kolkata, India

24.1 INTRODUCTION The global surge in the prevalence of overweight and obesity among children and adolescents over the past few decades is a serious concern, with a reported increase of 48.1% between 1980 and 2013 compared to a relatively modest increase of 27.5% in adults. Currently, up to 200 million school children are overweight, and 40 million are obese [1]. The number of infants and young children (aged 0–5 years) who are overweight has increased from 32 million globally in 1990 to 41 million in 2016 and, by current trends, is projected to be 70 million by 2025. More than 340 million children and adolescents from 5 to 19 years of age were overweight or obese in 2016 [2]. In low income countries (LICs), the prevalence of overweight is less compared to developed countries (6.1% versus 11.7%). However, the absolute number of obese children will be higher in the developing nations, and the rate of increase in overweight children in LICs is 30% higher yet, simultaneously, the majority of the children suffer from undernutrition and related problems. A recent global study on epidemiologic transition provides estimates of 333 disease conditions and injuries, and 84 risk factors from 1990 to 2016. Unhealthy dietary practices have emerged as an important determinant of Disability Adjusted Life Years (DALYs) (8.6%) along with childhood and maternal under nutrition (14.6%) and other factors [3]. A review of prevalence data from 52 studies conducted in 16 of the 28 states in India estimated a combined prevalence of 19.3% of childhood and adolescent overweight and obesity after 2010, which is significantly higher than the earlier reported prevalence of 16.3% from studies conducted between 2005 and 2010 [1]. A 2013 survey of 77,660 students aged 7–17years in 176 schools all over India found that about 38% students had body mass index (BMI) levels that were not age-appropriate. The results were similar from metro and semimetro cities, and in all regions of the country with reported prevalence of 37% (Central), 39% (East and North), 37% (South), and 38% (West) [4].

24.2 IMMEDIATE AND LONG-TERM CONSEQUENCES OF CHILDHOOD OBESITY Immediate consequences of obesity in childhood would include a multitude of effects on the orthopedic, pulmonary, gastrointestinal, endocrine, metabolic, and cardiovascular systems. Each component of the metabolic syndrome (MetS) worsens with increasing obesity at all ages. The prevalence of MetS in obese children and adolescents is as high as 36.6% in LICs [5]. Insulin resistance appears early, and type 2 diabetes driven by obesity is predicted to be the most common form of newly diagnosed diabetes in adolescent youth within another 10 years. Young type 2 diabetes patients are at an increased risk of nephropathy and retinopathy, as well as cardiovascular disease as compared to young people with type 1 diabetes [6, 7]. There is a significant association of obesity with hypertension in children and adolescents, predominantly systolic hypertension [8]. Left ventricular hypertrophy tracks from early childhood [9]. Markers of subclinical atherosclerosis, such as an increased carotid intima media thickness, are increased in obese children [10]. Obese adolescent females are at a particular high risk for hyperandrogenism and polycystic ovarian syndrome (PCOS) with all its consequences.

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Severe obesity poses a risk for orthopedic complications such as slipped capital femoral epiphyses [11], bowed tibia, Blount’s disease, and falls with fractures. Obese children often have moderate to severe obstructive sleep apnea with resultant pulmonary arterial hypertension. This is more common than the rare “obesity-hypoventilation syndrome” or Pickwickian syndrome. The association with bronchial hyperreactivity is debated, but diminished exercise tolerance for obese children when compared to the nonobese population is known. Gastrointestinal complications would include gallstones and a higher prevalence of steatohepatitis early in life. Rarely, such children might develop a raised intracranial tension due to pseudotumor cerebri. The psychosocial impact of childhood obesity can have significant negative consequences with body image disorder, adolescent or adulthood depression in males [12], and both depression and anxiety disorder in females [13] with poor self-esteem and even suicidal tendencies in some. Eating disorders are also common with predominantly bulimic behaviors in adolescence [14]. The major long-term consequences involve a progression to adulthood obesity, earlier onset and increased risk for dysglycemia and type 2 diabetes, dyslipidemia, atherosclerotic cardiovascular diseases (ASCVD), and nonalcoholic steatohepatitis. Adolescents with high normal BMI have been shown to have increased risk for ASCVD, nonatherosclerotic cardiovascular disease, colon cancer, and noncardia gastric cancer [15].

24.3 WHY IS PREVENTION IMPORTANT? • Pediatric Obesity Has Significant Short- and Long-Term Adverse Consequences, thus its prevention or reversal would be expected to yield significant benefits. • Limited Evidence of Efficacy and Safety of Pharmacologic Therapy in Obese Children: Pharmacologic interventions have not produced satisfactory results in the pediatric population compared to their adult counterparts. In addition, these are fraught with adverse consequences, limiting the number of adequately powered clinical trials that can be done to test their efficacy. As of now, there is insufficient evidence regarding the safety and efficacy for most of the antiobesity drugs in children, and most are not recommended by the existing guidelines [16, 17]. Intensive lifestyle modification forms the cornerstone of therapy in the obese pediatric population and has shown remarkably better results compared to adults. A similar albeit less stringent lifestyle intervention, if instituted prior to the onset of obesity, is likely to produce substantial benefits. • Exogenous Factors Leading to Obesity Are More Prevalent Than Endogenous Pathologic Conditions: Although a few endocrine, neurologic, and monogenic disorders and genetic syndromes conditions are linked with obesity in childhood, overall these account for only a small fraction of cases and often come to clinical attention for clinical manifestations unrelated to obesity. Most children suffer from so-called “exogenous obesity” due to a chronic mismatch between the energy intake and expenditure, and should be amenable to prevention.

24.4 RISK FACTORS FOR PEDIATRIC OBESITY The current epidemic of obesity is viewed as the result of gene-environment interactions—the “thrifty-gene” selection—in an attempt to deposit fat efficiently, which is maladaptive in this era of food overabundance.

24.4.1 Risk Factors in Fetal Life The “fetal origins hypothesis” proposes that certain aspects of the in-utero environment contribute to the development of obesity in small for gestational age (SGA), large for gestational age (LGA), and premature infants all of whom have fetal hyperinsulinemia and insulin resistance [18]. The risk is particularly high for SGA infants who demonstrate a rapid “catch-up” growth in the first 2–3 years of life. Maternal gestational diabetes mellitus (GDM) and poor glycemic control in diabetic mothers are known risk factors for an increased birth weight and also increased risk of overweight/ obesity from 4 to 8 years of age [19]. There is also a positive association with prepregnancy maternal BMI, maternal smoking, and an excessive gestational weight gain (GWG) [19, 20]. Studies have shown that small and thin Indian neonates have poor muscle and visceral mass but higher adiposity for a given weight compared to Caucasians. Overnutrition in a population with a genetic predisposition and history of multigenerational undernutrition increases maternal insulin resistance and promotes fetal adiposity [20].

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No candidate gene single nucleotide polymorphisms (SNPs) have been identified to identify “at-risk” individuals with certainty. The risk in fetal life is believed to be the effect of epigenetic modification on fetal programming [21].

24.4.2 Role of the Environment A multitude of environmental factors have been associated with childhood obesity based on the results of crosssectional epidemiologic studies, although an exact “cause-effect” relationship cannot be ascertained due to the lack of longitudinal studies. Many of the environmental risks have predominantly emerged in developing nations with increased globalization and improved economic status. Table 24.1 lists the environmental factors likely contributing to the obesity pandemic.

TABLE 24.1

Risk Factors for Childhood Obesity

Risk factors for childhood obesity [22, 23]

Special factors in LICs

Demographic factors

Ethnicity—African American, Hispanic, Native American race

Urbanization and residence in metropolitan cities

High socioeconomic status (SES) in LICs and low SES in high income countries (HICs) prepubertal age (?) and female gender

Increased exposure to westernized lifestyle in developing countries

Early introduction of complementary foods

Improved “purchasing power” and unrestricted access to energy-dense fast foods in school cafeteria, school vending machines, and school neighborhood due to improved affordability

Dietary habits

Formula feeds High intake of energy-dense foods Low intake of fruits and vegetables High intake of sugar-sweetened beverages (SSBs) and high fructose corn (HFC) syrups Large “portion sizes” Frequent midmeal snacking High glycemic index and low-fiber foods Low calcium diets (?) Low trace elements like Vd, Ch Parental feeding patterns Physical activity behavior

Sociocultural factors

Increased “screen time” and indoor leisure activities (television viewing, Internet, and computer games)

Lack of open spaces and playgrounds in schools and neighborhoods.

Increasing pressure on children to perform in academics and reduced emphasis on sports

Unsafe neighborhoods for walking and other outdoor activities

Commuting to school by bus or car instead of walking or bicycling

Easy availability of domestic help—no indoor activities

Lack of awareness regarding “healthy” food habits and need for physical activity

Forced feeding by parents and caregivers False traditional beliefs about health and nutrition

Aggressive mass-media advertisements of fast-food and colas Others

Poor educational status in parents and caregivers

Increased day-to-day stress—raised endogenous cortisol Sleep deprivation Medications—atypical antipsychotics, androgenic steroids

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FIG. 24.1 “Ecological systems theory” for childhood obesity. Adapted from Davison KK, Birch LL. Childhood overweight: a contextual model and recommendations for future research. Obes Rev 2001;2:159–71.

The problem of childhood obesity is multifaceted, and the role of the various environmental risk factors has been very nicely conceptualized by Davison and Birch using the Ecological Systems Theory (EST) as demonstrated in Fig. 24.1 [24]. A child stays in an ecological niche that includes the family and school, which in turn is embedded within a larger social context comprised of the community and society. According to this model, child “risk factors” include behavioral patterns involving diet, physical activity (PA), and sedentary behavior. The impact of these child risk factors is moderated by some nonmodifiable parameters such as age, gender, and a genetic susceptibility to weight gain. The development of these risk factors is determined by parenting styles and family characteristics that include parameters such as parents’ diet, activity patterns, knowledge regarding nutrition, child feeding practices, etc. Larger community and societal characteristics including school environment and access to recreational facilities can directly and indirectly influence the child’s weight status as a result of their effects on children’s diet and activity, and parenting habits, respectively. Many preventive strategies in the past have failed to show sustained results, likely because they were focused on any one or a few of the components of one particular level of this model. A proper understanding of this model helps in designing holistic preventive interventions that can be implemented across multiple contexts that have an influence on children’s eating, activity, and weight.

24.5 PRIMORDIAL AND PRIMARY PREVENTION The basics of a prevention strategy include food, PA, and knowledge.

24.5.1 Nutrition—Recommendations The Endocrine Society (ES) advocates healthy eating habits that include: • Avoidance of consumption of calorie-dense, nutrient-poor foods such as sugar-sweetened beverages (SSBs), sports drinks, fruit juices, so-called “fast foods,” foods with added table sugar, high-fructose corn syrup, processed foods with high-fat or high-sodium content, and calorie-dense snacks [17]. • Consumption of whole fruits instead of fruit juices; according to the American Association of Pediatrics (AAP), after 6 months of age, consumption of fruit juice should be limited to 4–6 oz per day; after 6 years of age, this might be relaxed to figures not exceeding 8–12 oz.

24.5.2 Physical Education—Recommendations ES recommends children and adolescents engage in at least 20 min, optimally 60 min, of moderate to vigorous PA at least 5 days/week. Moderate to vigorous exercise implies an energy expenditure of at least three metabolic equivalents (METs) [25]. Put simply, a moderate exercise is one that allows talking but not singing whereas vigorous exercise makes it impossible to

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sing and difficult to talk. Examples of moderate-vigorous exercise in a healthy person usually are brisk walking, dancing, swimming, or cycling on flat terrain [17]. 24.5.2.1 PA and Nutrition-Related Behavioral Modification This can be accomplished using comprehensive behavior-changing interventions at a family level and integrated with school- or community-based programs. Based on the results of successful randomized controlled trials (RCTs), the most promising behavior change techniques included [26]: • • • • • •

provision of individualized information regarding the consequences of obesity-promoting behaviors restructuring the environment to enable individualized behavior change guiding practices that would decrease the development of obesity identification of role models for behavior change implementation of stress management training providing general communication skills training

24.6 PRIMARY PREVENTION OF CHILDHOOD OBESITY: SETTINGS AND STRATEGIES The WHO identifies three broad components of approaches for population-based obesity prevention: structures within the government to support policies and intervention, population-wide policies, and community-based intervention strategies [27]. The community-based interventions can be employed at different settings based on the target age group and other societal parameters with a multitude of similar and different strategies in each setting. However, a multicomponent and multisetting intervention program is likely to be the most effective. Fig. 24.2 outlines the framework for the primary prevention of childhood obesity. Individual strategies in each of the settings are discussed in relevant sections. The majority of the evidence on obesity prevention strategies comes from studies in high income countries (HICs). However, the successful points that emerge are likely to be valuable in implementing similar interventions globally.

24.6.1 Community-Based Interventions 24.6.1.1 Child Care Settings As of now, there is weak-to-moderate evidence favoring the effectiveness of obesity interventions in the child care setting. However, current data suggest that more than 11 million children under 5 years of age spend and average 36 h per week in child care settings. These include institutions like preschools and daycare centers, or home care settings involving self-employed care providers. FIG. 24.2 Multilevel approaches to prevention of childhood obesity.

Approaches to childhood obesity prevention

Population wide Policies and legislation

Community based intervention

Settings

Home and family

Child-care

Schools

Community

Healthcare

Multi Setting

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Strategies for preventing childhood obesity specific to these settings have been developed that include recommendations for making water available throughout the day, limiting 100% fruit juice to 4–6 oz for 1- to 6-year-old children, avoiding sweets, providing nutrition education to children and their parents, promoting active daily play, limiting screen time, and encouraging caregivers to be role models of healthy dietary habits and PA. A few examples of programs successfully implemented in the child care setting include the Hip-Hop and Health Jr., the “Color me Healthy,” and the “Brocodile the Crocodile.” 24.6.1.2 School Settings In developed nations, up to 95% of youth aged 5–17 years spend around 6 h per day in schools. In India (https://www. smilefoundationindia.org/ourchildren.html), approximately half of all the school-age children actually go to school. Rural areas are poorly served. However, childhood obesity is mostly an urban phenomenon affecting higher socioeconomic status (SES) families. The CDC has laid down school health guidelines focusing on proper nutrition, physical activities, and health education as outlined in Table 24.2. Components of health education should include appropriate information on healthy eating and exercise as outlined in Table 24.3.

TABLE 24.2

School Health Guidelines

Summary of school health guidelines to promote healthy eating and physical activity Guideline 1

Use a coordinated approach to develop, implement, and evaluate healthy eating and physical activity policies and practices • Coordinate healthy eating and physical activity policies and practices through a school health council and school health coordinator. • Assess healthy eating and physical activity policies and practices. • Use a systematic approach to develop, implement, and monitor healthy eating and physical activity policies. • Evaluate healthy eating and physical activity policies and practices.

Guideline 2

Establish school environments that support healthy eating and physical activity • Provide access to healthy foods and physical activity opportunities and to sate spaces, facilities, and equipment for healthy eating and physical activity. • Establish a climate that encourages and does not stigmatize healthy eating and physical activity. • Create a school environment that encourages a healthy body image, shape, and size among all students and staff members, is accepting of diverse abilities, and does not tolerate weight-based teasing.

Guideline 3

Provide a quality school meal program and ensure that students have only appealing, healthy food and beverage choices offered outside of the school meal program • Promote access to and participation in school meals. • Provide nutritious and appealing school meals that comply with the Dietary Guidelines for Americans. • Ensure that all mods and beverages sold or served outside of school meal programs are nutritious and appealing.

Guideline 4

Implement a comprehensive physical activity program with quality physical education as the cornerstone • Require students in grades K-12 to participate in daily physical education that uses a planned and sequential curriculum and instructional practices that are consistent with national or state standards for physical education. • Provide a substantial percentage of each student’s recommended daily amount of physical activity in physical education class. • Use instructional strategies in physical education that enhance students’ behavioral skills, confidence in their abilities, and desire to adopt and maintain a physically active lifestyle. • Provide ample opportunities for all students to engage in physical activity outside of physical education class. • Ensure that physical education and other physical activity programs meet the needs and interests of all students.

Guideline 5

Implement health education that provides students with the knowledge, attitudes, skills, and experiences needed for lifelong healthy eating and physical activity • Require health education from prekindergarten through grade 12. • Implement a planned and sequential health education curriculum that is culturally and developmentally appropriate, addresses a clear set of behavioral outcomes that promote healthy eating and physical activity, and is based on national standards. • Use curricula that are consistent with scientific evidence of effectiveness in helping students improve healthy eating and physical activity behaviors. • Use classroom instructional methods and strategies that are interactive, engage all students, and are relevant to their daily lives and experiences.

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24.8 SECONDARY PREVENTION

TABLE 24.3

Principles of Healthy Eating and Physical Activity

Healthy eating

Physical activity

Focus on eating daily: • Eating variety of whole grain products, fruits and vegetables, and nonfat or low-fat milk or equivalent milk products • Eating appropriate amounts from each food group every day • Appropriate amounts of high-fiber foods • Drinking plenty of water • Limiting foods and beverages high in added sugar • Limiting the intake of fat, especially saturated and trans-fats • Eating breakfast every day • Eating healthy snacks • Eating healthy food when dining out • Preparing food in healthy ways • Supporting others to eat healthy

• Engage in moderate to vigorous physical activity for at least 60 min per day • Regularly engage in activities that increase cardiorespiratory endurance, flexibility, and muscle strength • Engage in warm-up and cool-down activities before and after exercise • Drink plenty of water before, during, and after physical activity • Follow a physical activity plan for healthy weight management • Avoid injury during physical activity • Support others to be physically active

24.7 PREVENTIVE STRATEGIES START IN-UTERO Because GWG of the mother is known to be an important predictor of obesity later on in the child; prevention strategies could start early in the fetal life by assuring that the mother gains weight as per the BMI-specific GWG recommendations in accordance with current IOM 2009 guidelines [28]. Further, healthy weight gain and healthy lifestyle habits could optimize pregnancy outcomes and prevent GDM. This reduces the chances of having an LGA baby, which itself increases future risk of obesity.

IOM 2009

Prepregnancy ΒMI category

Mean rate of weight gain in the second and third Trimester (kg week)

Recommended range of total weight gain (kg)

BMI < 18.5 kg/m2 underweight

0.5

12.5–18.0

2

0.4

11.5–16

2

BMI 25.0–29.9 kg/m overweight

0.3

7.0–11.5

BMI 30 kg/m obese

0.2

5.0–9.0

BMI 18.5–24.9 kg/m normal weight

2

Based on the majority of prenatal lifestyle intervention studies, however, have definite conclusions that suggests prevention of excessive GWG that may be linked to lower incidence of high birth weight cannot be established. However, all of these studies had the primary outcome of preventing excessive GWG and were underpowered to see the effect on the secondary outcome of preventing high infant birth weight. The study by Mottola et al. reported that, in overweight women, a significantly lower percentage of babies born weighing between 4 and 4.5 kg was found in the group following intense lifestyle intervention to control GWG, compared to controls (3.2% versus 18%, resp.; P ¼ .048) [29]. The most effective way of preventing excessive GWG is not clear, but a combination of prenatal interventions including nutritional counseling, supervised PA sessions, and a behavioral change approach might be the most successful. Importantly, SGA babies with rapid postnatal weight gain are at very high risk for future obesity and demands preventive strategies at this step by promoting breastfeeding and delaying introduction of complementary foods and high-protein intake diet during early childhood.

24.8 SECONDARY PREVENTION Strategies for secondary prevention of pediatric obesity would include early detection of the condition and halting or slowing the progression. The clinic visit is the ideal setting for secondary and tertiary prevention.

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24.8.1 Early Diagnosing Childhood Obesity A child or adolescent >2 years of age is overweight if the BMI is >85th percentile but <95th percentile for age and sex. The child is obese if the BMI is >95th percentile and is extremely obese if the BMI is >120% of the 95th percentile or >35 kg/m2 [17]. The BMI calculated should be plotted on the BMI-for-age percentile charts at least annually and reviewed at every visit. It is prudent to remember a few points while tracking the BMI for age. The normal pattern for BMI is to decrease from 2 years until 5–6 years of age and then to increase. The initial dip in BMI likely reflects a corresponding decrease in subcutaneous and total body fat percentage. The resulting V-shaped pattern is termed as the “adiposity rebound,” which falls between 4 and 7 years of age when BMI attains its nadir, followed by a progressive increase that persists through the rest of childhood and into young adulthood [22, 30]. Early adiposity rebound is thought to be a risk factor for the development of obesity later on. Also, the BMI developmental curve lacks an adolescent spurt due to differences in timing of the height and weight spurts. The commonly used CDC 2000 BMIfor-age percentiles are derived from US children from all racial/ethnic backgrounds, and they may not represent normal reference data for other geographic regions. The discrepancies in fat mass and body composition in South Asian adults when compared to Caucasians is an established fact and even in studies on adolescents. South Asian adolescents living in England have been found to have higher percentages of body fat than their peers of European heritage having the same BMI [31]. The other group of reference curves known as the International Obesity Task Force (IOTF) standards are derived from six pooled international data sets for children 2–18 years of age, and these assume that the most-appropriate cutoff points for overweight and obesity in children are those corresponding to the locations of BMI of 25 kg/m2 and 30 kg/m2, respectively, in the BMI distribution for adults [32]. Waist circumference in children can provide a better estimate of visceral adipose tissue, whereas BMI is better at estimating subcutaneous adipose tissue as assessed by MRI [33]. Waist circumference also seems to be a better predictor than BMI for insulin resistance, blood pressure, and serum triglycerides [34]. However, there is no data to identify waist circumference cutoffs that can appropriately identify children with the most visceral fat or who are at greatest risk for cardiovascular or metabolic problems. Consequently, it is not known exactly which waist circumference percentile clinicians should use and what clinical actions that value would indicate. Nevertheless, clinicians, especially those in subspecialty referral settings, may add waist circumference to the tools they use to assess risk. Because most schools mandate a set of uniforms, data on waist circumference can be obtained from tailors designated for making school uniforms without actually measuring waistlines at schools. Tailors can also provide information on neck girth, an emerging surrogate for upper body obesity. It is suggested that, in children, skin-fold measurements can perform as well as BMI or waist circumference to identify the fattest individuals or those with MetS. However, it is unclear whether it adds to the accuracy of risk assessment over and above BMI.

24.8.2 Clinical Assessment In overweight-obese children, history-taking should focus on • identifying an endocrine/neurologic/syndromic association • identification of modifiable lifestyle behaviors (e.g., dietary and PA practices) • assessment of current and future risks for medical comorbidities A discordance of height and weight velocities is found in almost all patients with an endocrine cause for obesity. Thus stigmata characteristic of a particular endocrine/syndromic disorder may help identify the cause and guide further targeted investigation, for example, for Prader Willi syndrome. In many of the monogenic causes, the target gene is seldom identified. Role of preventive measures in such disorders is limited. Dietary assessment should include traditional methods include 24-h recalls, food records, and food frequency questionnaires [35]. The 24-h recall should ideally be repeated on several separate occasions for a more accurate assessment. The patients write food records or parents based on what is consumed for several days including the amounts, recipes, and preparation methods. A food frequency questionnaire asks patients the frequency and portion size of specific foods they consume. A few rapid assessment tools like the Weight, Activity, Variety (In Diet), and Excess (WAVE) tool allow patients to evaluate eating behaviors and PA, and to deliver effective nutrition counseling [36]. An inquiry for contributors to relative excess energy intake including restaurant food, SSBs, 100% fruit juice, larger portion sizes, energy-dense foods, decreased fruit and vegetable consumption, and skipping of breakfasts should be made.

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Appropriate assessment of PA patterns can be made using questionnaires (self-report or interviewer-administered), direct observation, and electronic or mechanical monitoring (with a pedometer or mobile app) [37, 38]. However, most questionnaires are not validated for pediatric age groups although many focus on adolescents but are quite lengthy and not appropriate for use in the clinic setting. It is necessary to identify potential barriers to physical activities in children and adolescents, which include increased television watching or excessive stress of academics. Other issues are encouragement from parents, access for free-to-play organized sports, physical education classes, recess in schools, and safe and easily accessible playgrounds.

24.8.3 Treatment Intense lifestyle modification with the same principles as outlined in the primary prevention strategies form the mainstay of therapy for childhood obesity. Some studies have shown that lifestyle interventions are effective only when introduced before 10 years of age; earlier the age of intervention, better the long-term outcomes. Of the pharmacologic agents used to treat adult obesity, only orlistat is FDA-approved for obesity treatment in ages from 12 to 16 years [17]. Orlistat is an inhibitor of gastrointestinal lipase and, taken with meals, reduces fat absorption by 30% amounting to a BMI reduction of 0.7–1.7 kg/m2 [39]. However, its use is associated with significant gastrointestinal side effects including malabsorption of fat-soluble vitamins and fecal spotting [40]. Although metformin decreases fasting hyperinsulinemia and may promote weight loss when combined with a rigid meal plan, cessation of metformin therapy can lead to a rebound hyperinsulinemia and weight regain [41]. Overall mean decrease with metformin was only 1.16 kg/m2 over 6–12 months [42]. Studies in adolescents and children are limited. It can, however, be used in PCOS adolescents with impaired glucose tolerance and those on psychotropic agents [43, 44]. Side effects with metformin, including nausea, bloating, and diarrhea, at initiation of therapy are usually self-limited but may mandate discontinuation in some pediatric patients. Because of their adverse effects, abuse potential, and lack of trials showing long-term weight loss efficacy, the amphetamine-like agents are not recommended for obesity management in children and adolescents [17]. Growth hormone (GH) treatment of children and adolescents with Prader-Willi syndrome decreases body fat percentage and increases lean body mass [45]. Studies with somatostatin analogs like octreotide have reported weight stabilization rather than weight loss in children and adolescents with hypothalamic obesity [46]. The glucagon-like peptide 1 analog exenatide may potentially have efficacy in adolescent obesity. In a trial, when used for 3 months, exenatide reduced BMI by 1 kg/m2 versus controls [47]. Leptin therapy produces significant loss of fat mass when used in leptin-deficient patients [48]. Agents that have been recently approved for long-term obesity treatment in adults, such as lorcaserin or phentermine plus topiramate, currently lack pediatric-specific data [17]. In the largest adolescent trial with orlistat, those who decreased their body weight by >5% at 12 weeks progressed to decrease body weight further by 7.8% after 1 year of treatment; however, if the weight loss at 12 weeks was <5%, there was up to 2.3% weight gain after 1 year [49]. The recommendation is to discontinue medication when it appears relatively ineffective after 12 weeks or if a 5% decrease in BMI/BMI z-score does not occur [17]. The Task Force on Bariatric Surgery in adolescents who are extremely obese with serious comorbidities places a high value on amelioration of life-threatening complications and tends to discount surgical cost and perioperative complications. Adolescents appear to have greater rates of resolution of dysglycemia and improvement in other obesity-related comorbidities than adults, thus making bariatric surgery an interesting option in obese teens. However, given the potentially serious adverse consequences, bariatric surgery can be considered only when the patient has attained Tanner 4 or 5 pubertal development and final or near-final adult height, and if the patient has a BMI of >40 or >35 kg/m2 with significant comorbidities that persist despite a formal program of lifestyle modification, with or without pharmacotherapy [17].

24.9 TERTIARY PREVENTION This entails an early screening for the potential complications of obesity so as to allow a timely intervention. Table 24.4 provides a list of possible comorbidities or complications associated with pediatric obesity, the clinical pointers to their occurrence, and appropriate investigations to detect them early and grade their severity.

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Checklist for Monitoring of Complications and Comorbidities Associated with Childhood Obesity

Comorbidity/complications Obstructive sleep apnoea

Points to look for in clinical history and examination

Relevant investigations

Excess daytime somnolence with h/o snoring, arousal during sleep, and apneic spells

Polysomnography for AHI, RERA

Wheezing, dyspnea

Pulmonary function test, SpO2 and pCO2 measurement during sleep

NAFLD

Vague recurrent abdominal pain, hepatomegaly

USG liver, fibroscan, ruling out other etiologies of liver dysfunction ALT >25 U/L (boys) and >22 U/L (girls)

GERD

Heartburn, dysphagia

Upper GI endoscopy in selected cases

RUQ pain, vomiting

USG upper abdomen

Insulin resistant, type 2 diabetes mellitus,

AN, osmotic symptoms

FBS, PPBS (2 h post-75 g glucose), HbA1c-screening as per ADA guidelines; lipid profile

PCOS

Oligomenorrhea, hirsutism

TAS pelvis or TVS Serum testosterone, LH, FSH

Precocious puberty

Premature appearance of secondary sexual characteristics, testicular volume assessment

Serum Testosterone (boys), Estradiol (girls), LH

Hip/groin pain, arthralgia/waddling gait

X-ray hip

Knee pain

X-ray knees

BP monitoring with appropriate sized cuffs

ABPM, ECG, lipid profile

Flat affect, apathy

Comprehensive psychological assessment

Pulmonary complications asthma (?) obesity hypoventilation syndrome Gastrointestinal

Gall bladder disease +/ GB stones Endocrine

Orthopedic SCFE Blount’s disease Cardiovascular Hypertension Psychosocial Depression Anxiety Body image disorder

Body dissatisfaction, poor self-esteem h/o binge eating

Eating disorders

24.10 CHILDHOOD OBESITY: EXPERIENCE OF THE AUTHORS In the period 1996–2017, 2364 patients with obesity between the ages 5 and 18 years were seen. All gave consent for their data to be analyzed. Patients with syndromic obesity or with a secondary cause for obesity were excluded. Fig. 24.3 shows the distribution of males and females according to their BMI. Seventy of the 917 patients with overweight-obesity had PCOS and a majority had a BMI of 25–30 closely followed by a BMI of 20–25. The caregiver, usually a parent, was instructed to never serve food to the child. The child was instructed to serve herself, never take a second helping, and spend at least 20 min over a meal. The child was asked to eat in a fixed designated place, at fixed times, and not to use a TV or mobile phone while eating. No antiobesity pharmacotherapy was given, but coexisting problems were treated. Follow-up visits were scheduled every 6 months. BMI was calculated at each visit.

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REFERENCES

1000

609

876

315

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225 141

8

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0 20–25

25–30 M

FIG. 24.3

30–40

40–50

F

BMI wise distribution of males and females in our cohort.

FIG. 24.4

Mean change in BMI at each visit. Standard Deviation (SD) values are not included as the data is nonparametric.

Mean change in BMI 6 5.022222222

5 4 3 2 1

0.931578947 −0.472666667

0 0m

3 m–6 m

6 m–1 y

0 1–2 y

4.5–5.5 y

−1.157391304

Time since first visit

9.5–10.5 y

−1

Change in BMI from initial

5.52

−2

Results: A total of 2364 patients (1447 males and 917 females) were seen. Of these, 85% did not revisit. The reason for drop-out was lack of efficacy, ascertained through random phone calls. There was a significant fall of BMI in almost all the children who returned for follow-up. However over the next 5 years, all the responders had regained weight. The first 30 responders were chosen for further study. The BMI of these patients at baseline was paired with the BMI obtained on their next visit. Wilcoxon’s ranked sum test was used to compare the pairs. The fall in BMI between the first visit and the second (median 25.2–24.2 kg/m2) is statistically significant (P < .001). Longer-term follow-up of the patients, some over 5 years, showed that, in every instance, the BMI increased (Fig. 24.4). Discussion: A small subset (15%) of children appears to lose weight after physician-led counseling. Although the weight loss is not sustained, these children are motivated to attend on follow-up visits. When there is no initial weight loss, there is no motivation to return for follow-up. Thus the twin challenges are to produce an initial weight loss after counseling and then, later, to sustain it.

24.11 CONCLUSION Obesity constitutes the biggest pandemic of the century, and the rising prevalence of childhood obesity is of particular concern. The treatment options are limited and not without significant risks to the pediatric population, whereas the options for preventive measures are manifold and have a huge spectrum. The phrase “prevention is better than cure” probably holds the truest meaning when applied in connection with childhood obesity than any other disorder at present.

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