Pediatric and Adolescent Obesity

Pediatric and Adolescent Obesity
Edmond Pryce Wickham III
Melanie K. Bean
CASE STUDY
A 10-year-old girl is establishing care with you for ongoing primary care. At the visit, the patient’s mother expresses concern about her daughter’s increasing weight. The mother reports a steady weight gain over the past 6 years despite the daughter’s regular participation in sports and is concerned that her daughter may have an underlying medical condition responsible for her weight gain. The patient has a past medical history of asthma and previously received several courses of oral steroids; however, her asthma is currently managed with intermittent use of a beta-adrenergic agonist and she has not required an oral steroid in the past 3 years. There is no history of developmental delay or a learning disability, but the mother does note worsening school performance over the past 2 years that she believes is associated with increased teasing and bullying that the patient has experienced at school. The patient’s father has obesity, and there is a strong family history of type 2 diabetes mellitus (T2D). There is no family history of thyroid disease.
On physical examination, the patient’s height is 147 cm, weight is 53.6 kg, with a body mass index (BMI) of 24.8 kg/m2, and blood pressure is 119/78 mm Hg. Her examination is significant for mild acanthosis nigricans on her posterior neck, the absence of thyromegaly, and stage 3 breast and stage 2 pubic hair development. She had not had any previous laboratory testing.
CLINICAL SIGNIFICANCE
The prevalence of overweight and obesity in youth has increased dramatically, such that approximately one in five children in the United States would be classified as having obesity and one in three children having overweight.1 Youth with obesity are at significant risk of developing weight-related comorbidities over their lifetime, and such conditions may already be present during childhood and adolescence. Thus, the prevention, identification, and effective treatment of obesity by healthcare professionals (HCPs) caring for youth is paramount. In evaluating children and adolescents with obesity, the clinical assessment and management should be modified to account for the child’s specific developmental stage and physical development. This specific chapter will build on content from preceding chapters and highlight unique considerations in the assessment and treatment of pediatric obesity in the primary care setting including the appropriate classification of weight status in children, distinct components of the comprehensive pediatric obesity-focused assessment, and the importance of family-based change in behavioral weight management in the treatment of obesity in youth. In addition, the potential roles of pharmacotherapy and metabolic and bariatric surgery (MBS) in adolescents with severe obesity will be reviewed.
DEFINING PEDIATRIC OVERWEIGHT AND OBESITY
Classification of Weight Status During Childhood
As in adults, BMI is the recommended screening assessment of weight status in children aged 2 years and older.2,3 Although not a direct measure of body fat, BMI generally correlates with more direct and robust methods for measuring body fat in children and correlates with both concurrent and future health risks, including morbidity and mortality. Consequently, the calculation, documentation, and interpretation of BMI is recommended at least annually as part of routine pediatric health care.
However, the clinical interpretation of BMI in children is more complex than in adults, as weight and height are dynamic and anticipated to change as part of a child’s normal growth and development. Moreover, unlike other growth parameters, BMI does not simply increase from birth to adulthood. In fact, BMI is typically expected to decrease beginning in the second year of life, reaching a nadir at the age of 5 to 6 years, and then increase steadily throughout later childhood and adolescence. The vertex of this v- or u-shaped pattern in BMI trajectory is termed “adiposity rebound,” and children who experience adiposity rebound prior to 4 years of age are at increased risk of obesity later in life.4
In light of these normal developmental patterns, an absolute BMI value is typically not sufficient for characterizing weight and adiposity status in children and younger adolescents, and BMI percentiles specific for age and sex should be determined for children ≥2 years of age in the United States according to the revised 2000 Centers for Disease Control and Prevention (CDC) BMI data (https://www.cdc.gov/growthcharts/cdc_charts.htm). Age- and sex-specific BMI percentiles may be calculated by plotting the child’s calculated BMI on the appropriate CDC BMI chart (Figure 11.1). Alternatively, numerous online pediatric BMI percentile calculators are publicly available (https://www.cdc.gov/healthy-weight/bmi/calculator.html); many electronic medical records also contain automated functions for calculating BMI percentiles for pediatric patients.
The body weight status of a child or adolescent ≥2 years of age can then be classified according to the determined age- and sex-specific BMI percentiles (Table 11.1). Specifically, a BMI that is ≥85th percentile but <95th percentile is consistent with overweight, and a BMI ≥95th percentile (or an absolute BMI ≥30 kg/m2, whichever is lower) is consistent with obesity. Astute HCPs (and parents) may question how more than 5% of children can have obesity in light of the proposed definition (i.e., BMI ≥95th percentile). To avoid an upward shift in the weight- and BMI-for-age growth curves as a result of the secular increases in body weight that occurred during the 1980s and 1990s, the weight data for children aged 6 years and older used in the development of the 2000 CDC curves exclude data collected after 1980.
More recently, the classification of obesity in youth has been revised to include a definition for severe obesity (BMI ≥120% of the age- and sex-appropriate 95th percentile or an absolute BMI ≥35 kg/m2) in order to underscore the increased health risks of severe weight gain among children and adolescents.5 This category of severe obesity in youth has been further refined to include proposed definitions for Class 2 (BMI ≥120% of the age- and sex-appropriate 95th percentile or an absolute BMI ≥35 kg/m2) and Class 3 (BMI ≥140% of the 95th percentile or an absolute BMI ≥40 kg/m2) to coincide with adult definitions, as well as criteria for MBS in adolescents.1,2,6 Figure 11.2 contains specialized growth charts that can be used to determine pediatric obesity severity and class.5
Although increasing data support that rapid weight gain in early life and infancy may portend an increased risk of obesity in later childhood, the importance of an elevated BMI in children <2 years of age has not been definitively established.3 Moreover, both the CDC and the American Academy of Pediatrics (AAP) recommend using 2006 World Health Organization (WHO) growth standards (https://www.cdc.gov/growthcharts/who_charts.htm), as opposed to the 2000 CDC growth references, for assessing growth patterns for infants <2 years of age given the WHO growth standards’ more robust longitudinal data and inclusion of predominantly breastfeed infants.7 Even though the 2006 WHO growth standards include a BMI reference chart beginning at birth, the CDC-AAP expert panel does not recommend its clinical use before 2 years of age.7 Alternatively, guidelines have proposed that in children <2 years of age, a weight-for-recumbent length ratio ≥97.7th percentile according WHO growth standards may represent an appropriate definition of obesity2; however, the clinical utility of this definition remains unclear.
An additional approach that addresses the dynamic characteristics of BMI among youth is the use of BMI z-scores (or standard scores); a BMI z-score corresponds to the number of standard deviations that a given child’s BMI is away from the corresponding age- and sex-specific 50th percentile. However, even though automated pediatric BMI percentile calculators may also generate z-scores and BMI z-scores are frequently reported in the research literature, the clinical utility of a BMI z-score in direct patient care is limited.
Prevalence of Overweight and Obesity in Youth
Rates of overweight and obesity among US youth have increased substantially over the past 40 to 50 years across all age and racial/ethnic groups.1,2 According to the 2015-2016 National Health and Nutrition Examination Survey (NHANES) data, 18.5% of children in the United States aged 2 to 19 years have obesity and 35.1% have overweight.8 Prevalence rates of obesity among children and adolescents rise with increasing age and are slightly higher in boys compared with girls across age groups (Figure 11.3).8 Obesity also disproportionately affects African American and Hispanic youth; however, no racial/ethnic group is immune from the epidemic of pediatric obesity.8 Even though reported rates are lowest in Asian American children, there is concern that the proposed BMI percentile definitions of pediatric obesity may underestimate the health risks associated with increasing adiposity in this population.2
Although overall rates of obesity may be plateauing in some pediatric age groups,8 the prevalence of severe obesity continues to rise at alarming rates.1 Based on 2015-2016 NHANES data, 6.0% of US children aged 2 to 19 years have severe (i.e., Class 2 or higher) obesity. Prevalence estimates of severe obesity climb with age, with an estimated 9.5% and 4.5% of US youth aged 16 to 19 years meeting proposed definitions of Class 2 and Class 3 obesity, respectively.1
Health Impact of Overweight and Obesity During Childhood
Children with overweight and obesity are likely to have persistent obesity as adults. Based on the current prevalence of excess weight in youth, predictive modeling suggests that ˜50% to 60% of the current generation of US children will have obesity when they are 35 years old.9 Childhood obesity is associated with significant life-long morbidity and mortality, including an increased risk of T2D, cardiovascular disease, and premature death in adulthood.3,5,10 The risk for the development of many weight-related conditions in childhood (Figure 11.4) increases with obesity severity. Furthermore, pediatric obesity is associated with significant reductions in quality of life.11 As a result of obesity and the weight-comorbidities, a decline in life expectancy is projected, with today’s youth living shorter lives than their parents.12 Thus, the development of skills required for the compassionate and comprehensive care of youth with overweight and obesity, including an understanding of the complexities of the disease and evidenced-based treatment recommendations, is critical for all HCPs who care for children.
ETIOLOGY OF ABNORMAL WEIGHT GAIN IN YOUTH
As in adults, the etiology of the imbalance in energy metabolism that leads to excess weight gain in childhood is complex, resulting from the interactions of individual and family behaviors, environmental factors, and genetic susceptibility. Parental weight status is strongly associated with the offspring’s weight status, both when the offspring is a child and subsequently an adult. In fact, if a child has one parent with obesity, the child’s risk of obesity is increased three- to fourfold.13 Having two parents with obesity is associated with greater than a 10-fold increased risk of obesity in the child.13 The observed relation between parent and child BMI likely results from a combination of shared genetic and environmental factors; however, genetic factors appear to be the stronger contributor. Indeed, twin studies point to a heritability of up to 70% to 80% for BMI and adiposity.14 However, like other complex disease phenotypes, obesity results from the interplay of genetic predisposition which is most fully expressed in the setting of environmental triggers and exposures.
For the majority of youth with obesity, the genetic susceptibility toward excess weight gain is polygenic, resulting from the cumulative risk from multiple genetic loci, each accounting for relatively small variations in body weight.14 Discussions with patients and families should acknowledge the strong genetic contributions to obesity while promoting autonomy and self-efficacy in changing modifiable behaviors and factors within the obesogenic environment, which form the foundation of effective treatments and mitigate genetic risk. As there currently are no clinically useful genetic markers for obesity, HCPs should obtain a family history for overweight and obesity among family members.
Specific Genetic Conditions Associated With Obesity
Although severe early-onset obesity may result from single gene mutations or defects in specific chromosome regions, such conditions are rare.15 Nevertheless, providers should remain vigilant to clinical characteristics suggestive of underlying syndromic and monogenic etiologies that may be present. Specific diagnoses may convey additional health risks to affected individuals that warrant ongoing monitoring or impact clinical treatment recommendations and response. Most children with genetic syndromes associated with obesity manifest severe hyperphagia and have one or more suggestive clinical characteristics:
  • Neurodevelopmental abnormalities (e.g., developmental delay, intellectual disability, or behavioral concerns)
  • Phenotypic features (e.g., short stature, dysmorphic physical features, retinal dystrophy, deafness)
  • Associated endocrinopathies (e.g., hypogonadotropic hypogonadism leading to delayed puberty)
Syndromic Obesity
Prader-Willi Syndrome
The most common syndromic etiology of obesity is Prader-Willi syndrome (PWS), a multisystemic genomic imprinting disorder that results from the lack of expression of paternal genes located in the chromosome 15q11-q13 region, and affects approximately one in 10,000 to 30,000 individuals.16 Infants with PWS have significant hypotonia and feeding disorders. As a result, PWS may initially present as poor weight gain and failure to thrive during the first 2 years of life; the characteristic hyperphagia and associated severe weight gain typically emerge in later childhood.16 Clinical features of PWS to look for include
  • Significant hypotonia and feeding disorders at birth
  • Poor weight gain and failure to thrive during the first 2 years of life
  • Developmental delay and short stature and/or decreased growth velocity
  • Almond-shaped eyes, a thin upper lip, and small hands and feet (Figure 11.5)
Children with PWS typically experience hypogonadotropic hypogonadism and growth hormone deficiency. Recombinant human growth hormone (hGH) administration in youth with PWS results in increased height, improved body composition and physical strength, and beneficial cognitive effects.17 As a result, the early initiation of hGH therapy is recommend in infant and children with PWS, and evidence suggests ongoing benefits of hGH in adults with PWS.17 Consequently, HCPs caring for youth (and adults) with PWS should collaborate with a pediatric or adult endocrinologists as well as other specialists to ensure comprehensive care.
Bardet-Biedl Syndrome
The second most common syndromic etiology of obesity is Bardet-Biedl syndrome (BBS), a homozygous recessive multisystem disorder that affects an estimated one in 125,000 to 175,000 lives births.18 In addition to severe, early-onset obesity, other clinical features of BBS to look for include
  • Progressive visual loss as a result of a retinal disorder known as rod-cone dystrophy
  • Dysmorphic extremities including polydactyly, syndactyly, and brachydactyly (Figure 11.6)
  • Renal tract abnormalities including polycystic kidney disease
  • Learning disabilities, developmental delay, or intellectual disability
However, the clinical presentation of BBS is variable and may also include more severe developmental delay/intellectual disability, dysmorphic facial features including a prominent forehead or hypertelorism with deep-set eyes, dental abnormalities, hearing loss, hypogonadism (particularly among males), and ataxia with impaired coordination.18 With the exception of polydactyly, many of the signs and symptoms of BBS may not be readily apparent at birth, but begin to emerge during childhood or early adolescence. The variability in clinical phenotype in patients with BBS likely results from the fact that over 20 disease-causing genes have been identified, each encoding for proteins essential for the primary cilium/basal body complex.19 The primary focus of treatment in BBS is clinical and supportive management of syndrome-associated comorbidities including eye disease, kidney disease and obesity.19 Patients with BBS are also at increased risk of T2D, hypertension, and metabolic syndrome and should be screened and treated appropriately to mitigate accelerated decline in vision and kidney function. As with PWS, HCPs should collaborate with other specialists to ensure optimal care for individuals with BBS.
Monogenetic Obesity
Melanocortin 4 Receptor Deficiency
The most common monogenic cause of early-onset obesity is a heterozygous mutation in the gene encoding for the melanocortin 4 receptor (MC4R), a critical regulator of appetite and energy metabolism, affecting approximately 4% to 6% of patients with severe obesity.15,20 In contrast to most other monogenetic or syndromic etiologies of obesity, individuals with heterozygous MC4R mutations do not demonstrate short stature, developmental delay/intellectual disability or typical phenotypic features. Although accelerated linear growth in childhood and hyperinsulinemia may be subtle features associated with MC4R mutations, youth with obesity but without MC4R mutations may also manifest similar but less prominent growth acceleration and hyperinsulinemia.21 Given the lack of definitive characteristics besides early-onset, severe obesity, the clinical identification of individuals with MC4R mutations may be challenging without genetic testing (see below). At this time, the mainstay of treatment for patients with heterozygous MCR4 mutations is comprehensive lifestyle modification, with the potential addition of weight loss surgery.22 The FDA recently approved setmelanotide, a selective MCR4 agonist, for the treatment of rare genetic mutations upstream of MCR4. Although treatment of MC4R mutations was not included in the initial FDA approval, the agent’s role in individuals with minor MC4R defects is promising and warrants further investigation.23
Mutations in other single genes (e.g., leptin, leptin receptor, proopiomelanocortin [POMC] and proprotein convertase) may also result in severe, early-onset obesity, but these defects are extremely rare, typically associated with secondary endocrine dysfunction (e.g., central hypogonadism, adrenal insufficiency, or hypothyroidism), and not commonly encountered in clinical practice.24
When to Obtain Genetic Testing
Endocrine Society guidelines recommend consideration of genetic testing in patients with severe, early-onset obesity (before age 5 years) with clinical features of genetic syndromes and/or a family history of severe obesity.2 The diagnosis of PWS is confirmed by DNA methylation analysis, and DNA sequencing tests for MC4R mutations are commercially available. However, genetic testing/screening for etiologies of obesity, like other conditions, should be offered in the context of high-quality genetic counseling so that families and patients are well informed of the risks, benefits, and potential implications of testing. Parental permission for genetic testing should be obtained prior to testing, as well as assent from the child, when appropriate. Thus, genetic testing is ideally conducted in collaboration with dedicated genetic counselors and clinical geneticists, and referral is recommended.
Endocrine Conditions Associated With Obesity
Endocrine disorders such as hypercortisolism, hypothyroidism, and growth hormone deficiency may also result in excess weight gain, but these conditions are rarely the primary underlying cause of obesity in children.15 Moreover, youth with endocrine causes of obesity typically have other symptoms suggestive of the diagnosis beyond weight gain. An important clinical clue that may indicate an underlying endocrinopathy is short stature and, even more specifically, reduced height velocity.15 Thus, in addition to assessing trends in weight and BMI, the clinical evaluation of youth with obesity should include a careful review of the patient’s height growth. Many children with overweight and obesity experience slightly accelerated growth rates (i.e., height velocities) compared with healthy-weight peers during late childhood and early adolescence, such that 10- to 12-year-old girls and 11- to 13-year-old boys with overweight and obesity are ˜3 cm taller than same-sex youth with a healthy weight.25 However, the discrepancy in height between youth according to weight status is no longer apparent in older age groups as both groups approach their genetically determined adult predicted height.25
The early growth spurt and advanced skeletal maturation in children with obesity is likely driven, in part, by an early onset of puberty (and associated increase in sex steroids) in youth with excess body adiposity.26 Girls with overweight and obesity are more likely to experience earlier onset of breast and pubic hair development and menstrual periods.27 The relation between BMI, body fat, and pubertal development in male youth is less clear, with studies suggesting that boys with overweight/obesity are more likely to experience both early and delayed pubertal development.26,28 Elevated levels of insulin and leptin have also been implicated as contributing to the early weight-related growth acceleration in both sexes.26
Given the low prevalence of underlying endocrine conditions in asymptomatic youth with overweight and obesity, guidelines recommend against the routine laboratory evaluation for endocrine etiologies of excess weight gain (including thyroid function studies) unless the child has one of the following:2,3
  • An attenuated height velocity (or a height that is shorter than anticipated according to genetic and familial potential).
  • Clear signs or symptoms suggestive of an endocrine disorder beyond weight gain.
However, when the clinical assessment or testing suggests an underlying endocrine condition, referral to a pediatric endocrine specialist is warranted.
Hypothalamic Obesity
In light of the central role of the intricate central nervous system pathways involved in the regulation of appetite and energy metabolism, damage to these areas in the hypothalamus from tumors, surgery, radiation, trauma, or inflammatory disease may lead to marked obesity.29 Children and adolescents with hypothalamic obesity manifest severe hyperphagia as well as metabolic changes that result in reduced energy expenditure that can contribute to ongoing weight gain even in the setting of aggressive lifestyle modification and caloric restriction.29
CLINICAL EVALUATION OF PEDIATRIC PATIENTS WITH OVERWEIGHT AND OBESITY
As outlined previously, an assessment of weight status and obesity risk is recommended at least annually as part of routine pediatric care. Given the substantial lifetime risk of overweight and obesity as well as the central role of dietary intake and regular physical activity in health and chronic disease prevention, it is recommended that pediatric HCPs routinely and thoughtfully assess a child’s dietary and physical activity patterns, regardless of the patient’s current BMI. For children and adolescents with established overweight or obesity, the initial encounter should focus on
  • Establishing rapport with the patient and family.
  • Identifying any underlying etiologies contributing to excess weight gain.
  • Screening for the presence of weight-related comorbidities.
  • Age-appropriate assessment of dietary, physical activity, sedentary behaviors, and sleep patterns.
  • Collaboratively developing and implementing an age-appropriate, family-based treatment plan that accounts for the patient/family’s readiness to change, unique values, and goals.
Initiating Discussions Regarding Weight and Health Behaviors During Pediatric Encounters
Tragically, many youth with overweight and obesity face significant stigmatization and discrimination at home, in school, through media, and, unfortunately, with health care.30 Consequently, it is imperative that providers develop and refine a clinical approach and practice environment that minimizes weight-related stigma. One particular approach for establishing rapport and minimizing weight stigma is for the provider to ask permission prior to discussing weight and weight-related concerns. As with many aspects of pediatric care, providers should modify this approach to account for the developmental stage of the patient. For example, even when a parent of an older child or adolescent initiates a discussion with an HCP about weight, it is important for the provider to seek verbal assent from the patient as well.
Although pediatric guidelines recommend the use of the clinical terms of “overweight” and “obesity” for clinical documentation, experts recommend the use of different terms during clinical encounters to reduce stigma.3 In a survey of parents of children aged 2 to 18 years regarding perceptions of different weight-related terms used by HCPs, parents indicated that more neutral words like “weight,” “unhealthy weight,” or “high BMI” were more desirable, motivating, and less stigmatizing than terms like “heavy,” “chubby,” “obese,” or “fat.”31 It may also be helpful to review concerns regarding weight in the context of reviewing the patient’s growth chart: “Your child’s BMI has been increasing over the past several years and is now above the 95th percentile. What concerns, if any, do you have about his weight?”
In addition to the thoughtful selection of terms to describe weight during encounters, providers are encouraged to use open-ended questions initially to assess both the parent and child’s level of concern, followed by more direct, but still neutral, questions in order to gather additional aspects of the history. During this process, providers should consistently engage the child and adolescent as developmentally appropriate and practice reflective listening with both the patient and the caregiver.
Components of Medical History in Children With Overweight and Obesity
Weight History
The initial evaluation of a child or adolescent with overweight or obesity should include a complete medical history including details regarding the onset and pattern of abnormal weight gain. As outlined previously, severe early-onset obesity (before 5 years of age) may suggest an underlying syndromic or monogenic etiology. The sudden onset of weight gain should prompt providers to explore temporal relations to medication initiation or changes, significant changes in the social environment (e.g., change in residence, parent’s divorce, family member’s death), or the emergence of symptoms of disordered eating or another underlying medical problem. In addition, HCPs should inquire about previous efforts at behavior change (including who participated in the changes) as well as participation in dedicated obesity treatments including specific dietary interventions, community-based or structured weight management programs, or use of antiobesity medications.
Past Medical and Surgical History
A detailed past medical history should be obtained including the diagnosis and treatment of any weight-related comorbidities. The presence of other medical diagnoses (and associated pharmacotherapy) may not only increase the child’s risk of obesity, but also significantly impact the approach to obesity treatment. Detailed information regarding current and prior medication use, including the use of over-the-counter medications and vitamin/mineral supplements, should be obtained. Children with autism spectrum disorders, Fragile X syndrome, and trisomy 21 are more likely to have overweight and obesity, and individualized treatment plans for affected youth often need to account for strong food preferences, developmental delay/ intellectual disabilities, and/or behavioral challenges. Youth with attention-deficit hyperactivity disorder (ADHD) are also at increased risk of obesity, particularly those not receiving pharmacotherapy.32 For youth with a history of anxiety, depression, and other mood disorders, the clinical interview should also include a history of current and previous treatments and address both behavioral therapies and medication use. A complete review of systems (including snoring/sleep disturbances, headaches, abdominal pain, menstrual irregularities, hirsutism, hip/knee/leg pain, polyuria, polydipsia, depressed mood, and anxiety) should be obtained to assist HCPs in identifying any previously unidentified weight-related comorbidities and concerns.
Birth History
For younger children, details from the patient’s birth history and early life may provide information regarding obesity and other cardiometabolic disease risk. A maternal history of gestational diabetes mellitus during the pregnancy, maternal tobacco use, higher birth weight, and delivery via cesarean section are associated with increased risk of obesity in the child.33 Breastfeeding may be associated with lower risk of obesity in the child, and the introduction of solid food before 4 months of age may be associated with increased risk.33 However, the evidence regarding both of these early dietary risk factors is inconsistent.33
Developmental History
Collecting a developmental history, noting any delays in early language and fine and gross motor development, is vital and may provide clues to suggest an underlying syndromic or genetic etiology of the child’s weight gain. The developmental history should be expanded to include any concerns regarding attenuated growth velocity as well as a history of early or delayed pubertal development, as appropriate.
Family History
Family history should include the presence of family members with a history of overweight and obesity (as well as history of family members undergoing MBS), T2D, gestational diabetes mellitus, hypertension, dyslipidemia, and premature cardiovascular disease.
Social History
The social history should include an assessment of the child’s living situation; school performance including any learning disabilities or individualized educational programs (IEPs); daycare, before- and after-school supervision, and employment; and substance use patterns. As part of the social history, it is important to identify any caregivers besides parents (e.g., grandparents, sitter) who play significant roles in the child’s life who may need to be engaged in treatment plans. Given the association with childhood obesity (as well as pertinent implications to treatment plan development), an assessment of food security should be included. Although more comprehensive validated assessments are available, the inclusion of a single question (i.e., “In the last year, did you worry that your food would run out before you got money or food stamps to buy more?”) may identify a family with food insecurity. Unfortunately, weight-based bullying is highly prevalent, both at school and at home, and should also be assessed.30 A significant proportion of youth with obesity endorse being teased or bullied about their weight by a parent, and the clinical interview may be an opportunity for providers to model discussion using weight-neutral and nonstigmatizing language.
Assessment of Dietary and Physical Activity Patterns in Children
Other essential portions of the pediatric history include the identification of key modifiable behaviors related to energy metabolism, including an age-appropriate assessment of dietary and activity patterns.34 HCPs may find it beneficial use a screening questionnaire (Table 11.2) to collect such information. As with all components of the pediatric encounter, the patient should be engaged in dietary and activity pattern assessments as age and developmentally appropriate, using neutral and nonjudgmental language and an interview approach that reduces stigma. In addition, as part of the assessment of dietary and physical activity patterns, providers can also begin to partner with patients and families in the identification of specific target behaviors for reducing energy intake and increasing activity.
Dietary Assessments
Traditional dietary assessment measures such as a 24-hour dietary recalls, food records, and food frequency questionnaires have been validated for use in children and are often used in research studies. However, the use of these instruments in a busy clinical practice is typically not helpful. Instead, guidelines propose that providers assess several key behaviors that significantly impact energy intake in children including: (1) consumption of sugar-sweetened beverages (SSB), (2) frequency of food consumed outside of the home, especially at fast food restaurants, (3) portion sizes, and (4) frequency, quality, and setting of meals and snacks.34
Assessments of SSB should extend beyond soda/soft drinks and include consumption of juice, lemonade, flavored milk, sweet tea, sports drinks, energy drinks, and coffee-based beverages. The consumption of SSB in youth has increased dramatically over the past several decades, and mounting cross-sectional and longitudinal studies support a relation between SSB intake and weight gain during childhood and adolescence.35 Moreover, pediatric intervention studies have demonstrated that the elimination of calories from SSB leads to reductions in BMI.35 Thus, SSB intake represents a key therapeutic target when the patient and family are ready to make such changes.

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Jun 23, 2022 | Posted by in ENDOCRINOLOGY | Comments Off on Pediatric and Adolescent Obesity

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