Greetings

You have in your hands, or at your fingertips, the first edition of the American Academy of Pediatrics clinical practice guideline for evaluation and management of children and adolescents with overweight and obesity. Putting together this guideline was no small task, and the Academy is grateful to the efforts of all the professionals who contributed to the production of this document. This work is a true testament to their passion and dedication to combatting childhood and adolescent overweight and obesity.

The Subcommittee responsible for developing this guideline comprises a diverse group of professionals from a variety of disciplines representing both governmental entities and private institutions. Experts all, they are united by a common desire to provide the finest, most effective care and treatment to children and adolescents with overweight and obesity. Over the course of several months, the members of the Subcommittee reviewed the technical reports produced from the study review, then worked in concert to develop the Key Action Statements and Expert Consensus Recommendations contained within this guideline. These were crafted with meticulous care by the Subcommittee members, to align with current literature and to place appropriate emphasis on each statement.

While representing such a broad spectrum of perspectives, the members of this committee are all keenly aware of the multitude of barriers to treatment that patients and their families face. These barriers impact not only their access to treatment, but their ability to follow prescribed treatment plans. Whereas some patients are able to adopt the lifestyle changes and habitualize elements of their prescribed treatment plans, so many others struggle to do so for a wide variety of reasons. The members of the Subcommittee understand all of this. To assist with optimizing health equity and overcoming these barriers, guidance on a number of multilevel factors related to barriers to treatment have been included in this guideline. During the course of their work, members of the Subcommittee acknowledged that, although so much has been learned to advance the treatment of children and adolescents with overweight and obesity, there is still so much we have yet to discover. The Subcommittee recognizes the importance that future studies will play in advancing our knowledge and understanding of this chronic disease, knowledge and understanding that will lead to the development of new and more effective treatments. Specific discussion about the needs for future research are included in the guideline.

It is the fervent hope of every member of the Subcommittee that this guideline and the resources that accompany it will provide you with a more complete understanding of the issues, factors, and needs of patients combating overweight and obesity, as well as successful treatment options to assist them in their battle. This guideline and the resources that accompany it are not only for you, they are because of you, and all that you do to care for each and every patient as if they were the most important one. Because, as we all know, they are.

Be well,

Doug Lunsford, Family Representative

The current and long-term health of 14.4 million children and adolescents is affected by obesity,1,2  making it one of the most common pediatric chronic diseases.35  Long stigmatized as a reversible consequence of personal choices, obesity has complex genetic, physiologic, socioeconomic, and environmental contributors. As the environment has become increasingly obesogenic, access to evidence-based treatment has become even more crucial.

A significant milestone in the fight to counter misperceptions about obesity and its causes occurred in 1998, when the National Institutes of Health (NIH) designated obesity as a chronic disease. The NIH made a further commitment to necessary research in the “Strategic Plan for NIH Obesity Research,” released by the NIH Obesity Task Force in 2011.6  In 2013, on the basis of accumulating evidence, the American Medical Association recognized obesity as a complex, chronic disease that requires medical attention.7 

The scientific and medical community’s understanding of obesity is constantly evolving. Increased understanding of the impact of social determinants of health (SDoHs, see Definition of Terms section) on the chronic disease of obesity—along with heightened appreciation of the impact of the chronicity and severity of obesity comorbidities—has enabled broader and deeper understanding of the complexity of both obesity risk and treatment.8,9  Multiple randomized controlled trials and comparative effectiveness studies have yielded effective treatment strategies, demonstrating that, despite the complex nature of this disease, obesity treatment can be successful.10,11 

The knowledge and skills to treat childhood obesity have become necessities for clinical teams in pediatric primary and subspecialty care. For more than 2 decades, the American Academy of Pediatrics (AAP) and its members have had the opportunity to collaborate with multiple scientific and professional organizations to improve the clinical care of children with overweight and obesity. Notable milestones include the 1998 “Expert Committee Recommendations,”12  the 2007 “Expert Committee Recommendations,”1315  the creation of the AAP Section on Obesity and founding of the Institute for Healthy Childhood Weight, both in 2013; and the Institute’s “Algorithm for the Assessment and Management of Childhood Obesity” in 2016.16 

This is the AAP’s first clinical practice guideline (CPG) outlining evidence-based evaluation and treatment of children and adolescents with overweight and obesity.

This guideline does not cover the prevention of obesity, which will be addressed in a forthcoming AAP policy statement.

The CPG also does not include guidance for overweight and obesity evaluation and treatment of children younger than 2 years. Children under the age of 2 were not part of the inclusion criteria for the evidence review, because it is difficult to practically define and measure excess adiposity in this age group. The CPG also does not discuss primary obesity prevention, as no studies reporting results of obesity prevention interventions met the inclusion criteria for the evidence review.

Nonetheless, the topics of obesity prevention and evaluation and treatment of children younger than 2 years are very important to reduce this threat to children’s current and future health. Future CPGs may include these topics; in the meantime, information that may assist pediatricians and other pediatric health care providers (PHCPs) is included on the AAP Institution for Healthy Childhood Weight’s Web site (aap.org/obesitycpg). Further information on the CPG’s methodology and the writing committee’s approach is covered in subsequent sections.

The CPG contains Key Action Statements (KASs), recommendations based on evidence from randomized controlled and comparative effectiveness trials as well as high-quality longitudinal and epidemiologic studies. The CPG writing Subcommittee uses the term “pediatricians and other pediatric health care providers” to include both pediatric primary and specialty care physicians and other medical providers as well as allied health care professionals, since all will encounter and can intervene with children with overweight, obesity, and obesity-related comorbidities. An algorithm with these KASs is provided in Appendix 1.

The KASs are supplemented by Consensus Recommendations that are based on expert opinion and address issues that were not part of the supporting technical reports (TRs). These consensus recommendations are supported by AAP-endorsed guidelines, clinical guidelines, and/or position statements from professional societies in the field and an extensive literature review.

This CPG stands on the shoulders of the pediatricians, other PHCPs, clinical researchers, and other stakeholders who collaborated to create the previous Expert Recommendations, which have been valued sources of guidance for health care professionals, clinical systems, parents, and other key stakeholders. It is our hope that this CPG will further advance the equitable care of children and adolescents with this chronic disease.

Childhood obesity results from a multifactorial set of socioecological, environmental, and genetic influences that act on children and families. Individuals exposed to adversity can have alterations in immunologic, metabolic, and epigenetic processes that increase risk for obesity by altering energy regulation.1719  These influences tend to be more prevalent among children who have experienced negative environmental and SDoHs, such as racism.20  Overweight and obesity are more common in children who live in poverty,21,22  children who live in underresourced communities,23  in families that have immigrated,24  or in children who experience discrimination or stigma.2532  As such, obesity does not affect all population groups equally.33  This fact highlights the importance of understanding the role of SDoHs34  as well as the social context of children and their families in the etiology and treatment of overweight and obesity.

Children with overweight and obesity benefit from health behavior and lifestyle treatment, which is a child-focused, family-centered, coordinated approach to care, coordinated by a patient-centered medical home, and may involve pediatricians, other pediatric health care providers (such as registered dietitian nutritionists [RDNs], psychologists, nurses, exercise specialists, and social workers), families, schools, communities, and health policy.35  Obesity is long-lasting and has persistent and negative health effects, attributable morbidity and mortality, and social and economic consequences that can impact a child’s quality of life.3639  Because obesity is a chronic disease with escalating effects over time, a life course approach to identification and treatment should begin as early as possible and continue longitudinally through childhood, adolescence, and young adulthood, with transition into adult care.36,3941 

It is not uncommon for the differences in disease prevalence and outcomes among population groups to be described in terms of ethnicity, race, gender, and/or age and for these differences to be referred to as “disparities.”42  Disparity, however, only defines differences between groups without referring to inequities that cause these differences among populations (ie, “economic, civil-political, cultural, or environmental conditions that are required to generate parity and equality”42 ). Precisely because of the intertwining of inequities throughout the life course, health disparities can be found from maternal pregnancy outcomes through adolescence and, as such, can have an inevitable impact on childhood obesity.

This distinction between health disparities and inequities is particularly important when considering chronic disease, because: (1) obesity risk factors are embedded in the socioecological and environmental fabric of children’s lives; and (2) there is a danger of stigmatizing children with obesity and their families on the basis of race and ethnicity, age, and gender based on the disparities of outcome—with failure to recognize the systemic challenges that cause and maintain inequities.43,44 

Inequities are often associated with each other45  and result in disparities in obesity risk and outcomes across the socioecological spectrum. Importantly, they represent neighborhood-, community-, and population-level factors that can be changed.46  Inequities that promote obesity in childhood can have a longitudinal effect leading to disparities in adult health and contributing to adult obesity and chronic disease.47 

The AAP is dedicated to reducing health disparities and increasing health equity for all children and adolescents.28  Attainment of these goals requires addressing inequities in available resources and systemic barriers to quality health care services for children with obesity.48  To that end, “practice standards must evolve to support an equity-based practice paradigm” and payment strategies must promote this approach to care.28 

It is our hope that individual clinical encounters with patients and families will provide opportunities to “screen and address the social, economic, educational, environmental, and personal-capital needs of the children with obesity and their families.”49  In addition, understanding the wider determinants of the chronic disease of obesity will enable pediatricians and other PHCPs to “raise awareness of the relevance of these social and environmental determinants of childhood obesity in their communities.”49 

Racism as an SDoH has been defined as a “system of structuring opportunity and assigning value based on the social interpretation of how one looks (race) that unfairly disadvantages some individuals and communities (and) unfairly advantages other individuals and communities…”50,51  that “impacts the health status of children, adolescents, emerging adults and their families.”52 

Inequalities in poverty, unemployment, and homeownership attributable to structural racism have been linked to increased obesity rates.53  Racism experienced in everyday life has also been associated with increased obesity prevalence.54  Youth with overweight and obesity have been found to be at increased risk not only for weight-based harassment but also for sexual harassment and harassment based on race and ethnicity, socioeconomic status (SES), and gender.55  In adults, studies have found positive associations between self-reported discrimination and waist circumference,56,57  visceral adiposity,58  and BMI57  in both non-Latino and Latino populations.59 

Individuals with overweight and obesity experience weight stigma, victimization, teasing, and bullying, which contribute to binge eating, social isolation, avoidance of health care services, and decreased physical activity.28,43  Importantly, internalized weight bias has been associated with a negative impact on mental health.60  Collectively, these factors may adversely affect quality of care, prevent patients with overweight and obesity from seeking medical care, and contribute to worsened morbidity and mortality, independent of excess adiposity.28,43,44 

Pediatricians and other PHCPs have been—and remain—a source of weight bias. They first need to uncover and address their own attitudes regarding children with obesity. Understanding weight stigma and bias, and learning how to reduce it in the clinical setting, sets the stage for productive discussions and improved relationships between families and pediatricians or other PHCPs. Acknowledging the multitude of genetic and environmental factors that contribute to the complexity of obesity is an important mitigator in reducing weight stigma.61  Additional actions that reduce weight stigma include having appropriately sized office furniture, using appropriate capacity medical equipment, ensuring that aesthetic and/or instructional images posted in the office are inclusive, and avoiding stigmatizing language.28  Accordingly, the CPG utilizes person-first language (ie, using the term “child with obesity, rather than “obese child”) to avoid labeling the child.28  This practice is consistent with recommendations from the AAP and other national organizations, including the Academy of Nutrition and Dietetics, the Obesity Society, and the Obesity Action Coalition.62 

Adverse childhood experiences (ACEs) are negative experiences caused by situations or events in the lives of children and adolescents that can pose threats to their current and future physical and mental health.63,64  These experiences range from family turmoil and violence to financial hardship, loss of a parent, divorce, abuse, and parental mental illness—to name a few.65  ACEs have been associated with obesity, both in adulthood and in childhood.6668  Children and adolescents who live in poverty have a higher likelihood of experiencing ACEs, but risk for ACEs occurs at every income level.65,69  The greater the number of ACEs a child or adolescent experiences, the greater the risk for obesity.70  The most commonly cited mechanisms linking ACEs to obesity are social disruption, negative health behaviors, and chronic stress response.71 

Approach Summary

The recommendations in the CPG are child-centric and not specific to a particular health care setting and are written to inform pediatricians and other PHCPs about the standard of care for evaluating and treating children with overweight and obesity and related comorbidities. To reflect the pediatrician’s and PHCP’s individual relationship with the child and family, the Subcommittee refers to “evaluation” (eg, for comorbidities) rather than “screening.” It is anticipated that a pediatrician’s or other PHCP’s setting, training, and expertise may moderate how elements of the CPG are implemented. Helpful resources can be found in accompanying implementation materials.

Understanding the underlying genetic, biological, environmental, and social determinants that pose risk for obesity is the bedrock of all evaluation and intervention. Allowing the family to have a safe space to understand and process the complexity of obesity and its chronicity requires tact, empathy, and humility. Achieving this goal enables the patient and family to gain the knowledge and understanding needed to recognize risk factors in their environment and behaviors, to honor cultural preferences, and to institute changes independently as well as under the guidance of a trusted and well-trained advocate—such as pediatricians and other PHCPs.

Finally, to emphasize important goals of treatment—both improved weight status and reduction or elimination of comorbidities—the Subcommittee uses the term intensive health behavior and lifestyle treatment (IHBLT) rather than “intensive lifestyle or behavioral modification” or “weight management.” Additional definitions are listed in the next section.

BMI: BMI is a measure used to screen for excess body adiposity; it is calculated by dividing a person’s weight in kilograms by the square of height in meters. For children and teens, BMI interpretation is age- and sex-specific. A child’s BMI category (eg, healthy weight, overweight) is determined using an age- and sex-specific percentile for BMI rather than the BMI cut-points used for adult categories.72 

Capacity-building: “Building individual competencies and technical expertise, strengthening organizational capacities, and enabling supportive structural environments” to maintain or improve health services delivery.73 

Children with special health care needs: Children with special health care needs are those who have, or who are at increased risk for, a chronic physical, developmental, behavioral, or emotional condition and who also require health and related services of a type or amount beyond that required by children generally.74 

Chronic care model: The chronic care model identifies essential elements of a health care system that encourage high-quality chronic disease care: the community; the health system; self-management support; delivery system design; decision support, and clinical information systems.75 

Chronic disease: The Centers for Disease Control and Prevention (CDC) defines chronic diseases broadly as “conditions that last 1 year or more and require ongoing medical attention or limit activities of daily living or both.”76  Obesity is a chronic disease that results in altered anatomy, physiology, and metabolism—all of which adversely affect the physical and mental health trajectory of children and adolescents.77  The Obesity Medicine Association defines obesity as a “chronic, relapsing, multifactorial, neurobehavioral disease, wherein an increase in body fat promotes adipose tissue dysfunction and abnormal fat mass physical forces, resulting in adverse metabolic, biomechanical, and psychosocial health consequences.”78 

Comprehensive obesity treatment: Comprehensive obesity treatment (COT) (Fig 1) includes79,80 :

  • Providing intensive, longitudinal treatment in the medical home

  • Evaluating and monitoring child or adolescent for obesity-related medical and psychological comorbidities

  • Identifying and addressing social drivers of health

  • Using nonstigmatizing approaches to clinical treatment that honor unique individual qualities of each child and family

  • Using motivational interviewing that addresses nutrition, physical activity, and health behavior change using evidence-based targets for weight reduction and health promotion

  • Setting collaborative treatment goals not limited to BMI stabilization or reduction; including goals which reflect improvement or resolution of comorbidities, quality of life, self-image, and other goals related to holistic care

  • Integrating weight management components and strategies across appropriate disciplines, which can include intensive health behavior and lifestyle treatment, with pharmacotherapy and metabolic and bariatric surgery if indicated

  • Tailoring treatment to the ongoing and changing needs of the individual child or adolescent, and the family and community context

Comprehensive patient history: A comprehensive patient history includes a review of systems; family history; history of present illness; and appropriate nutritional, physical activity, and psychosocial history.

Family-based treatment: Family-based treatment centers on the role of family at each stage of child development, includes consideration of the family’s critical role in supporting child health, and understands the unique contextual elements that affect the patient and family and influence treatment.

Intensive health behavior and lifestyle treatment: IHBLT educates and supports families in nutrition and physical activity changes that improve weight status and comorbidities and promote long-term health. IHBLT is most often effective when it occurs face-to-face, engages the whole family, and delivers at least 26 hours of nutrition, physical activity, and behavior change lessons over 3 to 12 months. IHBLT is foundational to COT and should continue longitudinally. It should be provided in conjunction with pharmacotherapy and metabolic and bariatric surgery if these treatments are indicated. IHBLT may be available in the form of a defined program and may be offered in pediatrician and other PHCP offices, medical centers or health systems, or in partnership with community organizations.

Longitudinal care: Care provided by a group of health care professionals who monitor a patient’s weight and other health indicators over a length of time sufficient to be associated with health improvements. Longitudinal care is continuous and coordinated and should include a plan for transition into adulthood.

Overweight and obesity: Overweight is defined as a BMI at or above the 85th percentile and below the 95th percentile for children and teens of the same age and sex. Obesity is defined as a BMI at or above the 95th percentile for children and teens of the same age and sex.

Pediatricians and other pediatric health care providers: For the purpose of this CPG, pediatricians and other pediatric health care providers refers to a qualified primary or tertiary care medical provider operating within their scope of practice and providing clinical care to children and adolescents. Examples include physicians, nurse practitioners, and physician assistants. (This document also refers to dietitians, licensed psychologists, exercise specialists, and other health care professionals who are not practicing medicine in the same manner.)

Pediatric medical home: The “pediatric medical home” delivers accessible, continuous, comprehensive, patient- and family-centered, coordinated, compassionate, and culturally effective health care. In this venue, well-trained pediatric physicians known to the child and family deliver or direct primary medical care.81 

Pediatric obesity specialist or clinician with expertise: Pediatric obesity specialists and clinicians with expertise are health care professionals with additional training in pediatric obesity medicine. Training may take the form of certification programs specific to obesity, fellowship, or a focus during specialty training, such as within endocrinology or gastroenterology specialty training. It may also take the form of an informal apprenticeship combined with professional workshops. For the purposes of this document, such training occurs within the context of recognized health care professional organizations.

Person-first language: According to the CDC, person-first language emphasizes the individual, not their disabilities.82  Hence, this CPG describes “children with obesity” or “adolescents with overweight,” not “obese children” and/or “overweight adolescents.”

Severe obesity: The expanded definition of “severe obesity” includes Class 2 and Class 3 obesity.83 

  • Class 2 obesity (≥120% to <140% of the 95th percentile) or a BMI ≥ 35 kg/m2 to <39 kg/m2, whichever is lower based on age and sex

  • Class 3 obesity (≥140% of the 95th percentile) or BMI ≥ 40 kg/m2, whichever is lower based on age and sex

Social determinants of health (SDoHs): SDoHs are the conditions in the environments where people are born, live, learn, work, play, worship, and age that affect a wide range of health, functioning, and quality-of-life outcomes and risks. SDoHs can be grouped into 5 domains: economic stability, education access and quality, neighborhood and built environment, and social and community context.8,84,85 

Treatment intensification: Treatment intensification occurs through increased frequency of contact, increased length of treatment, or other means of increasing the dose of treatment. Treatment intensification could include additional health care professionals and/or additional methods, such as physical therapy, psychotherapy, medical nutrition therapy, pharmacotherapy, or metabolic and bariatric surgery.

In 2017, the CDC supported the AAP’s Institute for Healthy Child Weight (the Institute) to conduct an evidence review of obesity treatment and obesity-related comorbidities. The Institute identified a methodologist and convened an evidence review committee consisting of pediatricians and researchers with expertise in pediatric obesity etiologies, diagnosis, and management. This committee, which met regularly in 2018 to 2019, followed established methods (elaborated on below) to create 2 TRs, which capture the evidence review committee’s findings and detail the search criteria, systematic review process, and research history. One TR is on overweight and obesity treatment (https://doi.org/10.1542/peds.2022-060643) and the second is on overweight and obesity comorbidities (https://doi.org/10.1542/peds.2022-060643).

Staff from the Institute and the AAP’s Council on Quality Improvement and Patient Safety formed a CPG writing Subcommittee, comprising the methodologist and several evidence review committee members; a range of pediatric primary and tertiary care providers; behavioral health, nutrition, and public health researchers; a pediatric surgeon; medical epidemiologists from the CDC Division of Nutrition, Physical Activity and Obesity; an implementation scientist; a parent representative; and a representative from the AAP Partnership for Policy Implementation. Most Subcommittee members also have other national organization affiliations relevant to pediatric overweight and obesity.

The Subcommittee members were identified by the AAP and met regularly in 2019 and 2020 and virtually thereafter. Members were assigned sections and met virtually to complete their sections. Sections were reviewed by the chair or cochair and outstanding issues were resolved by group consensus. The parent member was an at-large member of all the writing groups and reviewed each section. Members’ potential conflicts of interest were identified and considered; no conflicts prevented Subcommittee members from participating in the CPG development process.

This review was designed to answer 2 overarching key questions (KQs). KQ1 was: “What are effective clinically based treatments for pediatric obesity?” KQ2 was: “What is the risk of comorbidities among children with obesity?”

The Subcommittee developed this focus based on the needs of pediatricians and other PHCPs and the evidence required to inform the future development of clinical practice guidelines. The review did not attempt to address treatment strategies for comorbidities (eg, hypertension [HTN], sleep apnea, type 2 diabetes mellitus [T2DM]), as other guidelines and reviews are available to guide such treatment.8690 

B.1. Rationale for KQ1: Intervention Studies

Pediatricians and other PHCPs are a trusted source of health information for parents, including on issues related to nutrition and physical activity, which are key components of obesity prevention and treatment. To meet this need, pediatricians and other PHCPs need to know the strategies that have high-quality evidence for effectiveness in preventing and treating obesity. Additionally, pediatricians and other PHCPs need guidance on which treatments are effective for their population and how to leverage available resources for obesity treatment efforts.

B.2. Rationale for KQ2: Comorbidity Studies

Previous recommendations have included assessments of comorbidities, including HTN, dyslipidemia, glucose, fatty liver disease, and others. It is not clear whether these assessments lead to improved treatment strategies or outcomes. Additionally, it is not clear whether conducting these assessments would result in an adverse outcome. We examined specific conditions that were previously recommended or that would reasonably require screening: dyslipidemia, HTN, diabetes, fatty liver disease, depression, sleep apnea, and asthma. This is not intended to be a comprehensive list of all conditions comorbid with obesity but represents those most common and for which screening is potentially helpful.

The Evidence Review Subcommittee searched PubMed and CENTRAL (for trials). The initial search was on April 6, 2018, and an additional search was conducted to update the review, covering the time period April 7, 2018 through February 15, 2020. Both searches followed the same procedures, which are described below.

The Subcommittee combined the searches for both KQ1 and KQ2 because of their significant overlap to more efficiently review studies. Because the focus was on interventions that are relevant to primary care, the Subcommittee did not search other discipline-specific databases, such as ERIC or PsycInfo.

The Subcommittee searched for studies of children or adolescents, with a focus on overweight, obesity, or weight status; involving pediatricians, other pediatric health care providers, health care, or other treatment or screening (KQ1); and examining common comorbidities (KQ2). For both questions, the Subcommittee limited only using key words, not filters, to ensure the inclusion of the newest studies that had not yet been fully indexed. No date limits were placed on searches. In practice, this meant the Subcommittee reviewed studies from 1950 to 2020, although fewer than 2% of the studies were from before 1980.

The complete search strategies are included in Appendix 2 of the accompanying TRs (https://doi.org/10.1542/peds.2022-060642 and https://doi.org/10.1542/peds.2022-060643).

D.1. Inclusion Criteria Common to All Studies

All studies were required to include children ages 2 to 18 years. Studies could also include young adults up to age 25, if this population was stratified from older adult participants, as long as children younger than 18 years were also included in the study. Children could have other conditions (eg, asthma), as long as these conditions were not known to cause obesity, or be taking medications (eg, steroids) other than those known to be significantly obesogenic. Conditions known to cause obesity, such as Prader-Willi syndrome, obesogenic medication (eg, antipsychotics), or known genetic mutations associated with obesity (eg, melanocortin 4 receptor [MC4R]) were excluded.

All studies had to originate from Organization for Economic Cooperation and Development member countries and be available in English.

The race distribution of the samples is reported in the accompanying technical report evidence overview (Appendix 5 in TRs [https://doi.org/10.1542/peds.2022-060642 and https://doi.org/10.1542/peds.2022-060643]) to assist in interpretation of evidence within a health equity framework. The technical report authors notated in the “special populations” section of Appendix 5 when each study specifically focused on a lower-resourced population, as well as race and ethnicity distributions for all studies.

The primary aim of the intervention studies had to be examination of an obesity prevention (intended for children of any weight status) or treatment (intended for children with overweight or obesity) intervention. The primary intended outcome had to be obesity, broadly defined, and not an obesity comorbidity. Studies of obesity interventions that reported other outcomes were included.

Interventions could involve any approach, including screening, counseling, medically managed weight loss, pharmaceutical treatment, or surgery. Regardless of the intervention components, there had to be some level of outpatient clinical involvement in the treatment (ie, not just referral to an outside program), such as screening or a clinic follow-up appointment. Interventions that occurred completely outside the scope of health care were excluded. For example, school-based obesity prevention programs or community-based activity programs with no pediatrician or other pediatric health care provider involvement were excluded.

The Subcommittee did not limit the search by study design but did report experimental and nonexperimental studies separately. Although nonexperimental designs were included, all studies had to have a relevant comparison group to be included in the TR on interventions (https://doi.org/10.1542/peds.2022-060642).

D.3. Inclusion Criteria for KQ2 (Comorbidity Studies)

The Subcommittee included studies that had a primary aim of comparing comorbidities among those with and without obesity or by severity of obesity. Obesity and the comorbidity had to be measured contemporaneously to reflect the practice of clinical screening. Obesity had to be categorized using a BMI-based measure into accepted categories (ie, healthy weight, overweight, class 1 obesity, class 2 obesity, class 3 obesity). These categories could be based on percentiles or z-scores and could use the distributions relevant to the studied population (eg, World Health Organization [WHO] or the CDC).91,92 

All studies had to include 1 or more of the following comorbidities: lipids, blood pressure (BP), HTN, liver function, glucose metabolism, obstructive sleep apnea (OSA), asthma, or depression. These were chosen based on known associations with weight and potential for screening in the primary care setting.

The complete inclusion criteria are included in Appendix 3 of the accompanying TR on comorbidities (https://doi.org/10.1542/peds. 2022-060643).

The Subcommittee used Covidence to manage the review process (https://www.covidence.org/). Covidence is a program for online collaboration and management of systematic reviews. All abstracts were reviewed by 2 independent reviewers on the Subcommittee, who assessed the study’s inclusion in the full-text review process. All conflicts were discussed and resolved. Articles excluded at this stage were assigned an exclusion reason, with a hierarchy, which is shown in Appendix 4 of the accompanying TRs (https://doi.org/10.1542/peds.2022-060642 and https://doi.org/10.1542/peds.2022- 060643).

All articles deemed to meet criteria for full text inclusion were categorized into different data extraction strategies. Randomized trials were given a quality assessment using the Cochrane Risk of Bias tool. The Subcommittee decided not to limit studies based on the study quality, because many of them did not reach “high-quality” status (ie, at low risk of bias for most or all domains in the Cochrane Risk of Bias Assessment) using any of the tools. This occurred largely because studies consisted primarily of behavioral interventions without the possibility of blinding.

All studies, regardless of group, were fully extracted by 2 reviewers, and conflicts were discussed and resolved. Intervention studies were categorized into 5 groups for data extraction.

F.1. Group 1 Extraction

Group 1 articles included randomized trials of diet or “lifestyle” interventions. Extraction of these articles included: sponsorship or funder, design, population information, provider type, detailed intervention strategies and intensity, and BMI-based outcomes. The Subcommittee also identified outcomes other than BMI, including lipids, glucose metabolism, BP, other laboratory values, other obesity measures, psychosocial outcomes, mental health, behaviors, and other outcomes (primarily parent BMI and child cardiovascular fitness).

The Subcommittee categorized the intensity of interventions in a manner consistent with the US Preventive Services Task Force (USPSTF) to allow for comparisons with its findings, into interventions with a dose (number of hours) of <5 hours; 5 to 25 hours; 26 to 51 hours; and 52 or more hours. All interventions occurred over less than 1 year. The Subcommittee conducted quality assessment for group 1 articles.

F.2. Group 2 Extraction

Group 2 articles included randomized controlled trials of pharmaceutical treatments. Similar information as above was extracted, using a brief description of the treatment and no categorization of intensity. These articles also received a quality assessment.

F.3. Groups 3 Through 5 Extraction

i) Groups 3 Through 5 Articles Group 3 articles included nonrandomized comparative studies of diet and “lifestyle” treatments, group 4 articles included nonrandomized comparative studies of pharmaceutical treatment, and group 5 articles included any surgical studies.

Because of small numbers, the Subcommittee combined randomized and nonrandomized surgical studies. Brief treatment descriptions and BMI-related outcome data were extracted from these, but the Cochrane Risk of Bias tool was not used because these were observational designs.

All studies were extracted by 2 reviewers who reported prevalence of comorbidities or mean values of laboratory parameters by weight classification. The Subcommittee included healthy weight, overweight, class 1 obesity, class 2 obesity, and class 3 obesity.

Because all classes of obesity severity were not always reported in the studies, these classes may include higher groups. For example, reporting of ≥95th percentile would only be considered class 1 obesity, although children at higher levels may be included. (See the TR for a detailed description of the KQ1 extraction procedures.)

The Subcommittee’s primary method of data synthesis was narrative. To allow broad inclusion, the Subcommittee did not limit to specific designs or measures that would facilitate meta-analysis. The Subcommittee has reported on studies in each group based on their type and design and has reported findings for outcomes other than BMI.

The AAP policy statement, “Classifying Recommendations for Clinical Practice Guidelines,” was followed in designating aggregate evidence quality levels for the available evidence (Fig 2).93  The AAP policy statement is consistent with the grading recommendations advanced by the University of Oxford Centre for Evidence-Based Medicine.

Evidence grades were determined based on the grading matrix in Fig 2. Although we included both trials and observational studies in the technical reports, they are reviewed separately. Study design was considered in the aggregate evidence quality grades, as indicated by the matrix. We did not explicitly use risk of bias scores, but this information was available and used in the Subcommittee’s final assessment.

The Subcommittee reached consensus on the evidence, which was then used to develop the clinical practice guideline’s KASs. When the scientific evidence was at least “good” in quality and demonstrated a preponderance of benefits over harms, the KAS provides a “strong recommendation” or “recommendation.” Clinicians should follow a strong recommendation unless a clear and compelling rationale for an alternative approach is present; clinicians are prudent to follow a recommendation but are advised to remain alert to new information and be sensitive to patient preferences (Fig 2).

Integrating evidence quality appraisal with an assessment of the anticipated balance between benefits and harms leads to a designation of a strong recommendation, recommendation, option, or no recommendation. Once the evidence level was determined, an evidence grade was assigned. AAP policy stipulates that the evidence supporting each KAS be prospectively identified, appraised, and summarized, and an explicit link between quality levels and the grade of recommendation must be defined.

Possible grades of recommendations range from “A” to “D,” with “A” being the highest:

  • Grade A: consistent level A studies;

  • Grade B: consistent level B or extrapolations from level A studies;

  • Grade C: level C studies or extrapolations from level B or level C studies;

  • Grade D: level D evidence or troublingly inconsistent or inconclusive studies of any level; and

  • Level X: not an explicit level of evidence as outlined by the Centre for Evidence-Based Medicine. This level is reserved for interventions that are unethical or impossible to test in a controlled or scientific fashion and for which the preponderance of benefit or harm is overwhelming, precluding rigorous investigation.

When it was not possible to identify sufficient evidence, recommendations are based on the consensus opinion of the Subcommittee members.

Obesity is a common, complex, and often persistent chronic disease associated with serious health and social consequences.94  Childhood obesity is typically defined as having a BMI of ≥95th percentile for age and sex.95  Severe obesity is defined as BMI ≥ 120% of the 95th percentile for age and sex. The percentage of US children and adolescents affected by obesity has more than tripled from 5% in 1963 to 1965 to 19% in 2017 to 2018.2  In 2017 to 2018, the rise in obesity prevalence slowed in children younger than 6 years of age, but increases continued among certain populations, including adolescents and non-Hispanic Black and Mexican American youth.4  A predictive epidemiologic model estimates that if 2017 obesity trends hold, 57% of children aged 2 to 19 years will have obesity by the time they are 35 years of age, in 2050.36 

Obesity prevalence increases with increasing age.3  For example, in 2015 to 2016, the prevalence of obesity in children aged 2 to 5 years, 6 to 11 years, and 12 to 19 years was 13.9%, 18.4%, and 20.6%, respectively.3  Among children younger than 6 years, there were no significant trends in obesity from 1999 to 2018 for those 2 through 5 years of age.4  For children 6 through 11 years of age, significant trends in obesity show an increased prevalence from 15.8% in 1999 to 2002 to 19.3% in 2015 to 2018.4  Similarly, among adolescents 12 through 19 years, trends show increased obesity in the same time period from 16.0% to 20.9%.4  The proportion of children and youth 2 to 19 years of age with severe obesity increased from 4.9% in 1999 to 2000 to 7.9% in 2015 to 2016.4,96  The prevalence of severe obesity in youth 12 to 19 years of age in 2015 to 2018 was 7.6%.4 

The COVID-19 pandemic has significantly affected the lives and routines of children and adolescents. In 1 analysis, the pandemic period was associated with a doubling in the rate of BMI increase compared with the prepandemic period.97  Obesity prevention and management efforts should routinely include health care provider screening for BMI, food security, and social determinants of health and increased access to evidence-based pediatric weight management programs and food assistance resources to mitigate such effects in the future.97 

Disparities exist among children and youth with obesity, including, but not limited to, lower level of parental education, lower income, less access to healthier food options and safe and affordable physical activity opportunities, and higher incidence of ACEs.70,98,99  For example, among 5345 children 6 to 9 years of age, those whose parents had lower levels of education had a greater odds of having obesity compared with children whose parents had higher levels of education (odds ratio: 1.78; 95% confidence interval [CI]: 1.36 to 2.32).100  A cross-sectional analysis of 111 799 children in Massachusetts at the school district level showed that for every 1 percentage point increase in the proportion of children with low SES, there was a 1.17 percentage point increase in the prevalence of obesity.101  Furthermore, children with disabilities, including those with intellectual disabilities, are at higher risk for developing obesity than their peers without disabilities.102 

Finally, among 43 864 children and adolescents aged 10 to 17 years old, the presence of 2 or more early ACEs was associated with an increased odds of obesity later in childhood and adolescence (odds ratio: 1.21; 95% CI: 1.02 to 1.44).103  Together, these disparities highlight the burden of obesity in children from families of lower SES and the need to provide strategies to minimize these inequities.

Disparities also exist in obesity prevalence across ethnic and racial groups. In 2015 to 2018, non-Hispanic Black children and Mexican American youth 6 to 11 years of age had a higher prevalence of obesity compared with non-Hispanic white children (22.7% and 28.2% vs 15.5%, respectively).4  An analysis of the Indian Health Services National Data Warehouse showed that in 2015, the prevalence of overweight and obesity in American Indian and Alaska Native (AI/AN) children and adolescents was 18.5% and 29.7%, respectively.104 

Among children 2 to 5 years of age from lower-income families enrolled in the Special Supplemental Nutrition Program for Women, Infants, and Children program, recent analyses indicate a modest but significant decline in obesity prevalence from 2010 (15.9%) to 2018 (14.4%).106  Among these children, obesity prevalence ranged across states from 8.5% to 20.2%; disparities persisted by race and ethnicity despite changes in prevalence over time.105 

In addition, children and youth with special health care needs (CYSHCN) have a higher prevalence of obesity and lower levels of physical activity compared with children having typical growth and development.106108  Among CYSHCN, a metanalysis of studies of adolescents with intellectual disabilities found a pooled odds ratio of obesity of 1.80 compared with adolescents with typical development.102 

Children with obesity commonly become adolescents and adults with obesity; severe obesity during adolescence increases the risk for severe obesity during young adulthood.109,110  BMI levels strongly track throughout childhood and adolescence and are predictive of high adult BMI.110 

Obesity puts children and adolescents at risk for serious short- and long-term adverse health outcomes later in life, including cardiovascular disease, including HTN; dyslipidemia; insulin resistance; T2DM; and nonalcoholic fatty liver disease (NAFLD).38,96,111113  Additionally, prediabetes in youth with obesity, compared with youth with normal weight, has been associated with elevated systolic blood pressure and low-density lipoprotein, and lower insulin sensitivity.114 

In addition to physical and metabolic consequences, obesity in childhood and adolescence is associated with poor psychological and emotional health, increased stress, depressive symptoms, and low self-esteem.115  Several studies have determined that children of some racial and ethnic groups have a greater prevalence of comorbidities associated with childhood obesity, including HTN, T2DM, hypercholesterolemia, and depression, compared with non-Hispanic white children.116120 

Obesity in childhood and adolescence is associated with health care utilization and costs. For example, the most common primary conditions that cooccur with a secondary diagnosis of obesity and may increase costs and utilization include pregnancy, mood disorders, asthma, and diabetes.121  A modeling study has estimated that the total lifetime medical costs for 10-year-olds with lifelong obesity to be in the range of $9.4 to $14 billion for that cohort alone.122 

Tracking obesity across the lifespan underscores the importance of primary and secondary prevention and treatment efforts early in life. These efforts include evaluating for obesity using BMI; identifying children at high risk and adolescents; providing or referring to evidence-based obesity treatments for children, youth, and their families; and addressing SDoHs.

Although KAS 1 was not explicitly studied and referenced by the TR, most of the TR studies implicitly included measurement of height and weight and calculation and plotting of BMI as part of the study procedures. Thus, the concept of appropriate measurement, calculation, charting, and tracking is implicit in research-based evidence included in the TR (eg, references123,124,126,130 ).

The gold standard measurement of body composition—dual-energy x-ray absorptiometry—to identify, locate, and quantify body fat, and can be expensive and difficult to implement. In clinical practice, BMI is frequently used as both a screening and diagnostic tool for detecting excess body fat because it is easy to use and inexpensive. BMI is a validated proxy measure of underlying adiposity that is replicable and can track weight status in children and adolescents.38,131,132  Because of its ease of use, BMI is also frequently used to follow a child or adolescent’s weight trajectory over time. The CDC BMI growth curves are frequently used to visualize BMI trajectory over time. Furthermore, BMI is often used to evaluate the success or impact of interventions to improve weight status.

For most individuals, BMI is generally well-correlated with direct measures of body fat, including skinfold thickness measurements, bioelectrical impedance, densitometry, and dual-energy x-ray absorptiometry.131,133139 

BMI has limitations, however, including high specificity and low sensitivity for detecting excess adiposity.132  BMI does not directly measure body composition and fat content and may under- or overdetect excess adiposity in certain racial and ethnic groups.140,141  Finally, children and adolescents who have high fat-free mass may have a high BMI and, as a result, be incorrectly classified as having overweight or obesity.142 

The CDC’s 2000 Growth Charts are based on NHANES data from the 1960s through the early 1990s and include age- and sex-specific BMI-for-age charts.143  The CDC Growth Charts provide a historical comparison of children’s weight status relative to a time before the current obesity epidemic during that healthier growth patterns predominated; thus, percentiles on the Growth Charts do not equate to the current population distribution of BMI. The CDC Growth Charts are recommended for clinically tracking BMI patterns among US children and adolescents aged 2 to 18 years; although the CDC Growth Charts can be used for adolescents aged 19 to 21 years, in practice, most pediatricians and other PHCPs transition to adult BMI calculation and categorization for patients older than 18 years.143 

“Overweight” is defined as a BMI at or above the 85th percentile and below the 95th percentile for age and sex; “obesity” is defined as a BMI at or above the 95th percentile for age and sex. “Severe obesity” is defined as a BMI equal to or more than 120% above the 95th percentile, which approximates the 99th percentile. The CDC Growth Charts were not intended to track growth of children with extremely high BMI values. Because of limited data on children and adolescents above the 97th percentile in the reference population, higher percentile curves could not be generated. Caution was recommended in extrapolation of percentiles beyond the 97th percentile, as this may generate unusual or unexpected results.144  In older adolescents, the adult cut-off of a BMI equal to or greater than 30 kg/m2 can be used to define obesity if this value is less than the 95th percentile BMI for age and sex.

Conversion of BMI percentiles to z-scores (a statistical measure that describes a value’s relationship to a population mean) derived from the CDC Growth Charts have historically been used for assessing longitudinalchange in adiposity over time among children and adolescents with obesity.127  The change in z-score, however, may not accurately detect meaningful changes in weight status or comorbidity risk over time, particularly for children and adolescents with severe obesity caused by compression of z-scores corresponding to extremely high BMI values into a very narrow range.145  Consequently, investigators have proposed and described various alternative options, including using the degree to which, expressed in percentage, a particular BMI percentile was above the 95th percentile, or the median, for age and sex (referred to as percentage above the 95th percentile, or percentage above the median, respectively).

The “extended” method for calculating BMI z-scores and percentiles at extremely high BMI values was developed to address these limitations. This method incorporates data on children and adolescents with obesity from more recent NHANES surveys to better characterize the BMI distribution above the 95th percentile while retaining the 2000 CDC Growth Chart BMI distribution below the 95th percentile.

The CDC and the AAP recommend that weight status in children up to 2 years of age be tracked using the WHO’s weight-for-length, age-, and sex-specific charts.146,147  Specialized growth charts for children and adolescents with certain conditions, such as trisomy 21, can provide useful growth reference information for special populations. These charts may, however, be limited, for example, by the small sample sizes used in developing them, which may not be representative of all children and youth with trisomy 21.148 

BMI is a useful evaluation measure to clinically identify children with overweight and obesity for appropriate treatment—such as family-based behavioral therapy—which can lead to improvements in BMI and related comorbidities.123,124,127130,149152 

Following comprehensive systematic reviews, the USPSTF issued a Grade B recommendation that pediatricians and other PHCPs screen children and adolescents aged 6 years or older annually for obesity—defined by BMI percentile—and offer, or refer children and adolescents to, a comprehensive, intensive, family-based behavioral treatment to improve weight status.79  (A “comprehensive, intensive behavioral treatment” was defined as a treatment of 26 hours or more over a period of 2 to 12 months.) (See Evaluation and Treatment sections.)

Furthermore, the AAP’s Bright Futures recommendations, which are based on systematic reviews and expert panels, offer prevention guidelines including annual assessment of BMI alongside dietary nutrition and physical activity counseling for children and adolescents starting at 2 years old127,153 (Appendix 2).

Appendix 2 describes the USPSTF recommendations, Bright Futures recommendations, and the recommendations reflected in this CPG’s KAS 1. All 3 sources recommend annual screening for excess weight using BMI, with the USPSTF beginning at 6 years old and both Bright Futures and this CPG beginning at age 2 years. For children or adolescents with a BMI ≥ 95th percentile for age and sex, the USPSTF provides recommendations for primary care providers to offer, or refer them to, a comprehensive, family-based weight management intervention. Bright Futures recommends that primary care providers screen for excess weight and provide dietary nutrition and physical activity counseling for all children and adolescents with either overweight or obesity (BMI ≥ 85th and <95th percentile for age and sex). Bright Futures also provides implementation tips and guidance for pediatricians and other PHCPs including, for example, providing counseling using motivational interviewing. Bright Futures offers guidance to states by offering a framework for meeting national performance standards under Title V. Finally, Bright Futures suggests how communities and families can support healthier lifestyles and prevention. This CPG recommends referral to evidence-based weight management interventions for all children 2 years and older who have a BMI ≥ 95th percentile for age and sex (see KAS 1, above).

The practice of annual BMI measurement at well-child visits is recommended and central to the management and tracking of overweight and obesity in children.127,153,154  Limitations to this approach include missed opportunities to track and manage weight changes that occur in less than a 12-month period.127,153  However, other visit opportunities can be used to assess BMI outside the well-child visit.153  This CPG’s KAS on evaluation, based on the evidence described above, and in concordance with USPSTF and the Bright Futures recommendations, continues to highlight the critical importance of annual evaluation for excess weight and the provision of, or referral to, evidence-based interventions, as indicated, to promote the health and well-being of all children and adolescents.

Despite its limitations, BMI is currently the most appropriate clinical tool to screen for excess adiposity and make the clinical diagnosis of overweight or obesity. Thus, the BMI must be communicated to the patient and family, as it guides next steps for comprehensive evaluation and treatment of obesity and related comorbidities. Weight-related discussions can be uncomfortable for clinicians who want to avoid stigmatizing children because of their shape or size. Avoiding this discussion may, however, cause delays or barriers to patients receiving evidence-based care. In addition, obesity stigma can result in patient avoidance of health care and disruption of clinician-patient relationships. There is evidence that having conversations about obesity can facilitate effective treatment.155157 

Three key factors can facilitate a nonstigmatizing conversation about weight with patients and families:

  1. Ask permission to discuss the patient’s BMI and/or weight.

  2. Avoid labeling by using person-first language (“Child with obesity”; not “obese child” or “my patient is affected by obesity; not “my patient is obese”).158 

  3. Use words that are perceived as neutral by parents, adolescents, and children. In several studies inclusive of diverse racial, ethnic, and rural and urban populations, preferred words include: “unhealthy weight, gaining too much weight for age, height, or health, demasiado peso para su salud (too much weight for his or her health).” Words perceived as most offensive include: “obese, morbidly obese, large, fat, overweight, chubby, or sobrepeso (overweight).”156 

Recognize that discussing BMI with children, adolescents, and families, even when using nonstigmatizing language and preferred terms, can elicit strong emotional responses including sadness or anger. Acknowledging and validating those responses, while keeping the focus on the child’s health, can help to strengthen the relationship between the pediatrician or other PHCP and patient and family to support ongoing care.159 

Obesity is a chronic disease that has a multifactorial etiology. Risk factors for overweight and obesity—many of which are SDoHs—include broader policies and systems factors; institutional or organizational (ie, school); neighborhood and community; and family, socioeconomic, environmental, ecological, genetic, and biological factors (Table 1).21,160  These individual, social, and contextual risk factors often overlap and/or influence one another and can operate longitudinally throughout childhood and adolescence, initiating weight gain and escalating existing obesity. Children and their families interact with their environment at all of these levels and have a unique and “insider’s” point of view that needs to be understood in delivering culturally sensitive care.161 

Pediatricians and other PHCPs need to be aware of the risk factors for pediatric obesity to provide early anticipatory guidance for obesity prevention, monitor their patients closely, and intervene early when weight trajectory increases.

The CPG authors recommend pediatricians and other pediatric health care providers:

  • perform initial and longitudinal assessment of individual, structural, and contextual risk factors to provide individualized and tailored treatment of the child or adolescent with overweight or obesity.

The larger macroenvironment—including societal attitudes and beliefs, government policies, food industry practices, and the educational and health care systems—can influence obesity risk.162  It is difficult to make or sustain healthy behavior changes in an obesogenic environment that promotes high-energy intake, unhealthy dietary choices, and sedentary behavior.

A.1. Marketing of Unhealthy Foods

Marketing of unhealthy food and beverages directed at children tends to negatively impact their dietary choices and behaviors.163166  Foods and beverages embedded in entertainment media have been shown to influence eating behavior choices of children and also increase consumption of foods during or after exposure to the embedded foods.167 

A systematic review and meta-analysis showed that even short exposure to unhealthy food and beverage marketing targeted to children resulted in in increased dietary intake and behavior during and after the exposure.168  Both younger children and male children (sex assigned at birth) tend to be more susceptible to the food and beverage marketing,168  and because of their stage of cognitive development, younger children are more likely to be susceptible to advertising and interpret it as factual.169,170 

Currently, marketing to children targets highly palatable relatively inexpensive energy-dense foods and beverages.166  This marketing occurs via television, websites, online games, at supermarkets, and outside schools.166  Children are, unfortunately, frequently exposed to foods of low nutritional values from advertisements; therefore, it is not surprising that they have preferential increase in consumption of foods of low nutritional value.167 

A.2. Underresourced Communities

Underresourced communities are settings in which obesity risk factors can predominate over health-promoting factors. Children and families in these settings may be unable to access fresh fruits and vegetables and safe physical activity spaces and may suffer from food insecurity.170172  Limitations in transportation, cost, affordability, and availability may reduce access to health care and obesity treatment. Families may be struggling with poverty, access to healthy foods, lack of social supports, racism, and/or immigration status. Understanding these contextual factors that impact each child and family is crucial in being able to provide compassionate and effective obesity treatment.

A.2.a. Socioeconomic Status

Obesity has been shown to disproportionately affect children and adolescents who have low SES.173175  Even though the prevalence of obesity has been stabilizing among US children overall, the rates continue to increase among children with low SES.173,176  According to the Children’s Defense Fund, the poverty rate among US children is alarmingly high.177 

A longitudinal analysis of predominantly non-Hispanic white children in the United States found that low SES before 2 years of age was associated with higher obesity risk by adolescence in both boys and girls; this analysis also indicated that the effect of early poverty endures later in life.178  Similarly, another study found that low SES in early childhood had a long-term impact on overweight and obesity.179  This study found that the risk of experiencing overweight or obesity in adulthood was not altered by either upward or downward mobility of poverty after early childhood,179  indicating the long-term effect of poverty-related stress in early childhood.

Low SES may also be associated with higher risk for obesity by increasing the child’s experience with toxic stress. In addition, poverty may limit access to healthy foods and opportunities for physical activity.180182  Another study of a large dataset of children followed longitudinally from 9 months of age to kindergarten entry showed that SES played a major role in BMI z-score gaps in Hispanic children, whereas rapidity of weight gain in the first 9 months “accounted for much of the disparity between white children and children” of other races and ethnicities (other than Hispanic children).180 

A.2.b. Children in Families That Have Immigrated

For decades, researchers have believed that despite poverty and other negative SES factors, recently arrived immigrants are healthier than their US-born counterparts. Recent studies, however, have examined large datasets in novel ways and now call this idea into question when it comes to children in families that have immigrated.183 

As families who have immigrated try to adjust to a new culture, they may adopt Americanized foodways, which are high in fat, sugar, and salt. This tendency could be heightened by children’s exposure to media advertising these foods and high-energy snacks and by reduced physical activity.184,185 

Patterns of childhood overweight and obesity among families that have immigrated vary substantially by both ethnicity and generational status. Immigrants to the United States generally originate from countries that have a lower prevalence of obesity, but as families acculturate to US eating and activity patterns, rates of obesity may increase. One study found that second-generation Hispanic immigrants were 55% more likely to have obesity than nonimmigrant white children, whereas first-generation Asian immigrants had a 63% lower risk of having obesity.180 

Several studies have indicated different patterns of developing obesity in Mexican-origin populations among adults and children. Obesity among adults of Mexican origin in the United States has been associated with longer stays in the United States and with being born in the United States versus Mexico, which are 2 proxies for acculturation. This pattern differs in children, in whom “significantly higher obesity prevalence has been observed for first-generation young adult males (ages 18–24) and adolescent females (ages 12–17).”186 

In addition, in some cultures, larger body sizes may be preferred as an indication of health and wealth.187  This cultural factor may make it more difficult for parents to understand the gravity of their children’s overweight or obesity. For this and many other reasons, it is vital to ensure that children and families who have immigrated and who are native-born have access to culturally competent health care.188 

A.3. Food Insecurity

The literature positing an association between food insecurity and overweight and obesity in children has been inconsistent when looking at general child populations. Children living in households with food insecurity have been found, however, to have higher BMI z-scores and waist circumference measurement and a greater likelihood of having overweight or obesity.189  The correlation between food insecurity and obesity has been found to be higher in adolescents, who may have had more exposure to food insecurity over their life-course.190  Female children appear to more at risk for obesity in food-insecure environments, compared with male children.191 

Food insecurity is highly associated with poverty, and the cost of fruits and vegetables192  and fast food have been found to influence consumption in low-income families193,194  and to be positively related to overweight in children.195  Associations between consuming more sugar from sugar-sweetened beverages, and less frequency of eating breakfast and eating dinner with family have also been noted in families with food insecurity.190,196  Family dynamics around feeding may change in situations of food insecurity and include pressure to eat as well as monitoring and restrictive eating practices.191,197  Experiences of food insecurity are stressful for children and families and may add to the burden of chronic stress, which can result in altered eating patterns in the direction of either restricting intake or increasing consumption of energy-dense foods.190,196 

The AAP and Food Research and Action Center’s toolkit, Screen and Intervene: A Toolkit for Pediatricians to Address Food Insecurity, is designed to help pediatricians identify and address childhood food insecurity (available at https://frac.org/aaptoolkit). The Toolkit assists pediatricians and other PHCPs to: (1) better identify children living in households struggling with food insecurity; (2) sensitively address the topic; (3) connect patients and their families to federal nutrition programs and community resources; and (4) advocate for greater food security and improved overall health of children and their families. The toolkit also includes the “Hunger Vital Sign,” a simple, validated 2-question tool that can be used in the clinical setting to evaluate for food insecurity (see link to toolkit above).

Environmental factors play an important role in obesity prevalence. Families’ dietary and physical activity opportunities and practices (mentioned above) are influenced by their neighborhoods (Table 1).

B.1. School Environment

Children spend most of their time in school. Therefore, schools play an important role in influencing children’s food choices and physical activity level and, ultimately, their body weight. For example, the presence of fast foods, vending machines, and/or sweetened beverages in schools may negatively influence children’s food choices.198 

Systematic reviews have shown an association between fast food outlets and convenience stores located near schools and obesity in children.199,200  When analyzed by subgroups, a positive association has been seen between fast-food outlets and proximity to schools among Hispanic, Black, and white children. Although the association was seen for all grade levels, the effect was larger in younger grades.199  This review also reported a stronger association between fast-food outlets and grocery stores located near schools and obesity in socioeconomically underresourced neighborhoods.

B.2 Lack of Fresh Food Access

A neighborhood’s food environment has been shown to have mixed association with children’s BMI. Although some studies have shown that a 1.6-km distance or shorter from a home to a supermarket is associated with a lower BMI,201  other studies have found that the greater the number of supermarkets located near a child’s home, the higher the child’s BMI.202  Similarly, a systematic review reported mixed association, with some studies showing a negative association between supermarket accessibility and childhood and adolescent obesity, and other studies either showing a positive effect or no association.203 

Some of the differences were attributed to variations in assessment measures and lack of adjustment for confounding variables. Hence, it is not only the presence of supermarkets that is important, but also other factors that may impact dietary choices—such as the type of foods stocked, pricing, etc. Some, but not all, studies have reported a positive association between neighborhood poverty and childhood and adolescent obesity.204 

It has been suggested that lack of access to fresh fruits and vegetables may be a risk factor for childhood and adolescent obesity, as it may lead to an increased reliance on, and consumption of, unhealthy foods. The data for this association have been inconsistent, however. A recent systematic review showed that, although there was a negative association between access to fresh fruits and vegetables and healthy eating behavior, the association between access to fresh fruits and vegetables and overweight and obesity was inconclusive.205 

B.3. Presence of Fast-food Restaurants

Fast-food restaurants generally serve relatively low-priced and calorie-rich fast foods with high levels of saturated fat, simple carbohydrates, sugar, and sodium. Because of their easy availability, taste, and marketing strategies, fast foods tend to be popular with children and adolescents.206 

Fast-food consumption has been associated with weight gain.207  Some, but not all, studies have shown an association between access to fast-food restaurants and pediatric obesity.208  A meta-analysis and recent systematic review showed a mixed association between access to fast-food restaurants and weight-related behaviors and weight status in children and adolescents.209  This association was shown to be stronger in populations with lower SES.209 

B.4. Access to Safe Physical Activity

A child’s environment may influence the amount of physical activity they get. For example, living in an urban environment that lacks safe walkable and/or green spaces in which children can play may result in decreased physical activity levels. Greater exposure to green space has been shown to be associated with higher levels of physical activity and lower risk of obesity.210 

A recent systematic review of the literature on the influence of the built environment and childhood obesity found significant association between childhood obesity and traffic air pollution and indicators of walkability (which included intersection density and presence and amount of park area in the neighborhood).211 

In addition to green spaces, other aspects of the environment—including safety—are important in these spaces’ use. A study of low-income preschool children in New York City reported an association of lower obesity risk in neighborhoods with trees alongside the streets and a positive association between obesity and higher homicide rates in the neighborhood.212 

B.5. Environmental Health

Exposure to environmental hazards during the prenatal period, infancy, and childhood can have impacts on the health and well-being of children. Endocrine-disrupting chemicals (EDC) can cross the placental barrier and affect the fetus.213  There are some data that show an association between prenatal exposure to bisphenol A and polyfluoroalkyl and childhood obesity.214,215 

In the postnatal and infancy period exposure may occur through breastfeeding, inhalation, ingestion, or absorption through the skin. Children get exposed to chemicals that are used in household products including cleaning agents, food packaging, pesticides, fabrics, upholstery, etc. Leaching of chemical products (eg, bisphenols, phthalates, parabens, and other EDCs) has been reported in baby feeding bottles, clothing, diaper creams, etc. Exposure to EDCs during early childhood can affect programming of several systems, including endocrine and metabolic systems, which may affect BMI, cardiovascular, and metabolic outcomes later in life.213 

The family’s dietary preferences and lifestyle habits have a crucial role in influencing the child’s weight.216  Parenting feeding practices and modeling of eating behavior and the type and quantities of foods and beverages in the home have been reported to be important influences in children’s appetitive behaviors and food preferences.217 

C.1. Parenting Feeding Styles

Parenting styles differ and may have an impact on a child’s risk for obesity. Four types of parent feeding styles have been described: authoritative (responsive and warm with high expectations); authoritarian (not responsive but with high expectations); permissive or indulgent (responsive and warm but lenient with few rules); and negligent (not responsive with few rules). The 4 parenting styles discussed were initially defined by Baumrind (1966) and later expanded by Maccoby and Martin (1983).218,219  (Restrictive feeding was not included as 1 of the parenting styles.)

Authoritative feeding, where parents respond to the child’s cues of hunger and satiety, is considered to be protective against excessive weight gain. Children from authoritative parenting homes have been shown to eat more healthy foods, be more physically active, and have healthier BMI, compared with children raised in homes with authoritarian, permissive or indulgent, or negligent parenting styles.220,221 

One possible mechanism of parenting style’s influence on a child’s weight status is thought to be from interference in the child’s ability to self-regulate their dietary intake. An authoritarian parent, for example, may not respond to a child’s cues for energy intake, resulting in poor ability on the part of the child to self-regulate their own energy intake, and a higher likelihood of overindulging when presented with an opportunity to eat.222,223 

A large cross-sectional study showed that, among preschool- and school-aged children, authoritarian or negligent parenting is associated with a higher risk of obesity,224  whereas authoritative parenting was associated with healthy BMI.221  Among preschoolers, the effect of the parenting feeding style was found to be modulated by poverty, with the effect only being seen among children who were not living in poverty.224 

C.2. Family Home Environment Organization

A systematic review of associations between the organization of the family home environment and childhood obesity found that greater organization of the home environment, which included practices such as having family routines and setting limits, was inversely associated with obesity.225  This relationship was present for younger and older children. Most but not all of the 32 studies included in the review controlled for sociodemographic factors.

C.3. Sugar-Sweetened Beverages

A systematic review of 20 prospective cohort studies and randomized controlled trials from 2013 to 2015 found that sugar-sweetened beverages (SSBs) were positively associated with obesity in children in all but 1 study (96%).226  Based on this review and others demonstrating a link between SSB and multiple other medical and dental diseases, the AAP published a policy statement on SSBs in 2019, calling for broad implementation of policies restricting SSB consumption in children and adolescents.227 

C.4. Portion Sizes

Much of the research on the influence of portion size on children’s intake has been performed in laboratory settings providing a single meal to preschool-aged children. A comprehensive review of this research reported that children who serve or are served larger portions of commonly liked energy-dense foods typically consume larger amounts but cautioned that long-term studies of the effects of larger portions over time on a number of variables, including body weight, are lacking.228 

C.5. Snacking Behavior

A recent systematic review of body fat and consumption of ultra-processed foods (defined as snacks, fast foods, junk foods, and convenience foods) in children and adolescents found a positive association but noted that longer-term studies examining the association of these foods and obesity are needed.229 

C.6. Dining Out and Family Meals

Eating outside of the home has been shown to be associated with higher energy intake in both children and adults.230,231  In the United States, food eaten outside the home is characterized by higher fat content, larger portions, and greater energy intake.230 

In a systematic review of pediatric and adult studies, eating at fast-food establishments was associated with much higher weight gain, compared with eating at other types of restaurants.231 

Take-away food has also been associated with high BMI.231  Hence, eating outside of the home—irrespective of the type of restaurant establishment visited—is associated with higher risk of weight or BMI gain. Conversely, 2 meta-analyses found that increased frequency of eating family meals was associated with lower risk of childhood obesity.232,233 

C.7. Screen Time

Some, but not all, studies report an association between screen time duration, childhood adiposity,234236  and adult BMI.237  Some studies have shown a dose-response effect of screen time and childhood adiposity,235  with screen time greater than 2 hours per day being positively associated with higher risk of overweight or obesity.236  A recent meta-analysis reported 42% greater risk of overweight or obesity with more than 2 hours per day of television (TV) compared with 2 or fewer hours.238 

There is evidence to support the association between screen time and consumption of unhealthy diet and high energy intake.235  The appearance or depiction of food items while engaging in screen time may affect a child’s dietary behavior. A systematic review examining food choice and intake showed that food included in entertainment media affects eating behaviors of children.167  Children and adolescents are more exposed to food and beverage advertisements when watching TV.239  Additionally, increase in screen time may displace physical activity and interfere with sleep.235,240 

Although “screen time” includes TV, computer, video or videogames, mobile phones, and other digital devices, the majority of the studies published examined the effect of TV viewing.235  Male children and adolescents tend to spend more time on media screen devices and other Internet technology than female children and adolescents do.236 

C.8. Sedentary Behavior

The association between sedentary behavior and adiposity has been shown to range from small to inconsistent.241  Studies examining the effect of sedentary behavior alone on weight using accelerometer measures have shown no association between sedentary behavior and obesity. Teasing out the effects of sedentary behavior alone in treatment studies may be challenging, as this is often confounded with other behaviors such as physical activity, screen time, or increased intake of unhealthy foods.241 

C.9. Sleep Duration

Short sleep duration is associated with higher risk of obesity in children.242244  A meta-analysis of prospective cohort studies demonstrated a dose-response inverse association between sleep duration and risk of childhood overweight and obesity.244  Children 13 years and younger with short sleep duration (∼10 hours) had a 76% increased risk of overweight or obesity compared with their counterparts with longer sleep duration (12.2 hours).

Sleep restriction may be associated with increased calorie consumption.245,246  Additionally, fatigue and decreased physical activity has also been associated with short sleep duration. It is unclear whether the inverse association between sleep and adiposity is causal or a consequence of hormonal or metabolic disturbance.247  Although the exact mechanism for this association is unknown, some of the consequences of short sleep duration include hormonal and metabolic alterations—such as increased ghrelin and decreased leptin—which may lead to increased hunger.242 

C.10. Environmental Smoke Exposure

Children exposed to environmental tobacco smoke (ETS) have been found to have higher BMI compared with their nonexposed counterparts, according to a systematic review of ETS exposure and growth outcomes in children up to 8 years of age.248 

C.11. Psychosocial Stress

Psychosocial stress in the prenatal period may have an effect on endocrine function (hypothalamic-pituitary-adrenal axis and glucose–insulin metabolism) in the child’s life course. A meta-analysis showed that prenatal psychological stress was associated with higher risk of childhood and adolescent obesity.249 

Psychosocial and emotional issues may lead to weight gain through maladaptive coping mechanisms, including eating in the absence of hunger to suppress negative emotions, appetite up-regulation, low-grade inflammation, decrease in physical activity, increase in sedentary behavior, and sleep disturbance.154,250,251  Depression has been shown to be a risk factor in both pediatric and adult obesity.251  The association between depression and obesity could be reciprocal, as obesity may increase depression risk.

C.12. Adverse Childhood Experiences

A number of studies have documented an association between ACEs and the development of overweight and obesity. ACEs impact occurs via toxic stress, which occurs “when a child experiences strong, frequent, and/or prolonged adversity—such as physical or emotional abuse, chronic neglect, caregiver substance abuse or mental illness, exposure to violence, and/or the accumulated burdens of family economic hardship—without adequate adult support.”252,253 

ACEs include a history of physical, emotional, or sexual abuse; exposure to domestic violence; household dysfunction from parental divorce or substance abuse; economic insecurity; mental illness; and/or loss of a parent because of death or incarceration.69,254257 

A US study found that cumulative ACEs doubled the risk of children having overweight or obesity, compared with their counterparts with no history of ACEs.258  Unresolved stress and emotional issues may result in maladaptive coping strategies—such as binge eating, eating in the absence of hunger, impulsive eating, and poor sleep hygiene—which may result in further weight gain.

Poverty and associated toxic stresses in utero and early childhood have been suggested to initiate neuroendocrine and/or metabolic adaptations that produce biological phenotypes and obesogenic behaviors that lead to obesity.259,260  These effects may persist throughout the lifetime.260 

D.1. Genetic Factors

Heritability studies suggest that there is a 40% to 70% genetic contribution to an individual’s obesity risk.261263  Genome-wide association studies have identified 32 loci of significance to obesity predisposition.264  Genetic causes of obesity include both common and rare genetic variants that involve impairment of gene expression or function.264 

D.1.a and D.1.b. Monogenetic Syndromes and Polygenetic Effects

Polygenetic causes of obesity are by far the most common, and single gene defects are rarer causes of obesity. For example, MC4R, a heterozygous mutation, is the most common form of monogenic obesity and accounts for only 2% to 5% of severe obesity in children.265,266  Polygenic inheritance refers to a single inherited phenotypic trait that is controlled by 2 or more different genes. Polygenic variants, on their own, have little effect on an individual’s phenotype. The phenotypic effect manifests only in the presence of, or in combination with, other predisposing factors.

Children with genetic causes of obesity may present with characteristic clinical features that have historically included findings such as short stature, dysmorphic features, developmental delay, skeletal defects, deafness, retinal changes, or intellectual disability. It is important to note that more recently discovered genetic disorders associated with obesity are not necessarily characterized by these findings in childhood; for instance, short stature is not a hallmark of leptin deficiency in children. Table 2 lists selected monogenetic causes and syndromes associated with obesity.

Early onset of severe obesity and the presence of hyperphagia are the 2 clinical characteristics that distinguish genetic disorders of obesity. “Early onset” refers to the presence of obesity before age 5. As noted previously, “severe obesity” is defined as BMI ≥ 120% of the 95th percentile for age and sex. “Hyperphagia” is the presence of insatiable hunger in which the individual’s time to satiation is long, the individual’s duration of satiation is shorter, the individual’s feelings of hunger are prolonged, and the individual has a severe preoccupation with food and experiences distress if denied food.267 

D.1.c. Epigenetic Factors

Epigenetic factors can result in alterations in gene expression without alteration in genetic code. These epigenetic factors may modify the interaction of environmental and individual factors in promoting weight gain.269  One of the critical periods in the establishment of the epigenome is considered to be during embryonic development.270  Prepregnancy maternal or paternal obesity, for example, may influence epigenetic changes during subsequent pregnancy, increasing the risk of overweight or obesity in the offspring.269  Other risk factors during pregnancy—such as gestational diabetes or maternal excessive weight gain—may result in epigenetic changes and increase the risk of obesity in the offspring.

D.2. Prenatal Risk Factors

The perinatal environment plays an important role in a child’s later development of overweight or obesity. The mechanisms by which the fetal environment predisposes to the development of obesity are complex and poorly understood. They probably include gene-environment interactions or epigenetic changes attributable to several environmental factors, including maternal diet, physical activity, and/or other environmental contaminants.271,272 

Preterm infants have a greater likelihood of developing childhood obesity.273275  Although the exact mechanisms for this association are uncertain, several risk factors have been postulated, including feeding patterns leading to accelerated weight gain in preterm infants.273 

D.2.a. Parental Obesity

Parental weight is a strong predictor of pediatric obesity. Children are at greatest risk of developing obesity as an adult if at least 1 of their parents has obesity.276  A meta-analysis reported an increased risk of adolescent excess adiposity if either parent had overweight or obesity; the risk increased if both parents had obesity.277  Contributors to this association include genetic, environmental, and behavioral factors or the interaction of these factors, resulting in intergenerational transmission of adiposity.

Maternal BMI is a stronger predictor of childhood and adolescent obesity, compared with paternal obesity.247  Maternal obesity more than doubles the risk of adult obesity (see below). Paternal obesity has been associated with childhood and adolescent obesity and has an additive effect to maternal obesity.278 

D.2.b. Maternal Weight Gain

Prepregnancy adiposity and weight gain during pregnancy are associated with neonatal, infancy, and childhood adiposity.247  The known effect of maternal weight on the offspring led the Institute of Medicine (IOM) to recommend different ranges for weight gain during pregnancy, varying from 12.5 to 18 kg for underweight women to 5 to 9 kg for women with obesity (BMI > 30 kg/m2).279  Yet, between 1997 and 2007, almost half of pregnant US individuals gained more than the weight recommended by the IOM.280 

Excess maternal adiposity has been suggested to affect fetal metabolic programing and make the offspring more vulnerable to the obesogenic environment and increase the risk of obesity. This effect was illustrated in metabolic and bariatric surgery studies, in which children born to mothers with obesity after gastric bypass surgery had lower prevalence of macrosomia and severe obesity at adolescence, compared with their siblings born before the mothers’ surgery.247  Fetal or infant macrosomia and gestational diabetes are some of the complications associated with maternal obesity and serve as risk factors for later onset of obesity and T2DM in the offspring.281 

The exact mechanism by which maternal obesity predisposes to adverse outcomes in the offspring is unclear. It has been suggested that the pathways that are affected control the central regulation of appetite and insulin sensitivity and cardiovascular regulation.281  Alteration of the fetal hypothalamic-pituitary-adrenal axis function has been implicated in programming the metabolic syndrome of the offspring of mothers with obesity.282 

D.2.c. Gestational Diabetes

Infants and children of mothers with gestational diabetes mellitus (GDM) have higher fat mass and BMI than their counterparts whose mothers did not have GDM.283  Adjusting for maternal BMI and other potential confounders, GDM was shown to be associated with childhood obesity with odds ratio of 1.6 to 2.8.284,285  The odds of developing higher waist circumference (≥95th and percentile) in children of mothers with GDM was also found to be higher after controlling for potential confounders (OR, 1.55; 95% CI, 1.03–2.35).285  Sibling studies controlling for shared genetics and environment have shown higher BMIs in offspring exposed to diabetes in utero compared with their unexposed siblings.286 

Although the exact mechanisms of the effect of GDM are not fully understood, it has been postulated that the effect may be mediated through insulin. Pregnant women with GDM have higher insulin resistance compared with pregnant women without GDM.287,288  It has been suggested that maternal insulin resistance and hyperglycemia causes fetal hyperinsulinemia, resulting in excessive fetal growth with associated macrosomia and increased adiposity.287  Maternal hypertriglyceridemia from insulin resistance has also been thought to lead to increased adiposity and birth size even when glucose levels are well-controlled.289  Additionally, maternal diabetes is associated with increased leptin synthesis in the offspring.290  Epigenetic changes in infants of mothers with GDM is another suggested mechanism, affecting gene expression regulation body fat accumulation or other related metabolic pathways.291 

D.2.d. Maternal Smoking

Exposure to ETS has been shown to increase the prevalence of childhood and adolescent obesity.292294  A systematic review and meta-analysis reported an association between prenatal ETS and childhood and adolescent obesity; children exposed to ETS in utero had about 1.9 times greater risk of developing obesity, compared with their nonexposed counterparts.295  Prenatal exposure to the risk from tobacco smoke can occur both directly from smoking mothers and indirectly through ETS, although maternal smoking was found to more strongly predict obesity.

Children exposed to smoking in utero have a dose-dependent increased risk of developing overweight and obesity.296 

D.3. Postnatal Risk Factors

As with the prenatal environment, the postnatal environment is important to the later development of overweight and obesity. In addition to epigenetic mechanisms, behavioral habits begin to get set at an early age. Acceptance of foods, availability of high calorie foods, establishment of the microbiome, and early eating habits are only a few of the proposed mechanisms for postnatal factors to influence later weight status.297 

D.3.a. Birth Weight

Several studies have shown a U-shaped or J-shaped distribution between birth weight and adult BMI.247  Infants with both low (<2500 g) and high (>4000 g) birth weight have been shown to have higher risk of obesity, compared with infants with birth weight between 2500 and 4000 g.298  A high BMI and central adiposity are more prevalent among low-birth weight infants.299  Maternal prepregnancy weight and nutritional status are strong predictors of neonatal outcomes, with underweight prepregnancy increasing the risk of preterm birth and small-for-gestational-age neonates.300  Maternal pregnancy overweight and obesity are significantly associated with large-for-gestational-age babies.300 

D.3.b. Early Breastfeeding Cessation and Formula Feeding

Some, but not all, studies have reported decreased risk of childhood and adolescent obesity in breastfed infants.247  The majority of evidence is derived from observational studies and may include confounding effects.247  Some studies have reported that, compared with bottle-fed infants, breastfed infants are better able to regulate their energy intake and have lower risk of childhood excess weight gain.301  Other studies have also shown that body weight gain is slower in breastfed infants.247 

Breastfeeding has been found to be inversely associated with overweight risk in the first year of life, independent of maternal BMI and SES. Breastfeeding cessation before 6 months was associated with an increased risk of rapid weight gain and overweight by 12 months of age, compared with exclusive breastfeeding.302 

A systematic review of feeding practices associated with rapid infant weight gain found that certain practices (such as overfeeding, inappropriately concentrating formula, placing infants in bed with a bottle, or adding cereal to a bottle) may lead to rapid infant weight gain.303  In addition, infants fed high-protein formulas are at greater risk of elevated BMI later in childhood.247,304 

D.3.c. Rapid Weight Gain During Infancy and Early Childhood

In resource-abundant countries, rapid weight gain in infancy and during the first 2 years of life is associated with higher risk of obesity both in later childhood and in adulthood.247,305  A systematic review and meta-analysis found that children who experienced rapid weight gain from birth to age 2 were up to 3.6 times more likely to have overweight or obesity in childhood or adulthood, with the relationship being stronger between rapid infant weight gain and childhood overweight or obesity.306 

Therefore, rapid weight gain in infancy and early childhood can be viewed both as a risk factor for later excess weight gain and also as a signal, as mentioned previously, for pediatricians and other PHCPs to look for other underlying risk factors and causes for excess weight gain. For instance, early introduction (at younger than 4 months of age) of complementary foods has been found to increase the risk of childhood obesity in several systematic reviews.307,308 

D.3.d. Early Use of Antibiotics

Literature on antibiotic exposure in early life (<2 years) is mixed, with some suggestion that it may slightly increase the risk of childhood and adolescent obesity.309312  The association is stronger with repeated antibiotic exposure,313,314  exposure within the first 6 months of infancy,314  and broad-spectrum antibiotic use.310  With similar antibiotic exposure, boys appear to be more susceptible to weight gain than girls.295  Gut microbiota is usually established during the first years of life; it is hypothesized that the effect of antibiotics is mediated through the alteration of the gut microbiome, which plays a role in energy balance.

D.4. Childhood Risk Factors

Various medical conditions that present in childhood and adolescence are associated with the development and progression of overweight and obesity. Similarly, certain behaviors established in childhood and adolescence can increase the risk of later development of overweight and obesity.

D.4.a. Endocrine Disorders

Endocrine disorders account for less than 1% of all the causes of pediatric obesity. These disorders can be associated with endogenous or exogenous glucocorticoid excess (eg, Cushing syndrome, use of corticosteroid medications). Short stature or growth failure and abnormally high BMI may result from pseudohypoparathyroidism type 1a, growth hormone deficiency, or hypothyroidism.268,315 

D.4.b. Children and Youth With Special Health Care Needs Impacting Nutrition and Physical Activity
D.4.b.1 Children With Developmental and Physical Disabilities

A survey of data from NHANES, the National Health Interview Survey, and the National Survey of Children’s Health found that children with disabilities were from 27% to 59% more at risk for obesity than children without disabilities.316 

In addition to factors experienced by children without disabilities, factors that affect children with disabilities that have been implicated in their greater obesity risk are: more difficulty breastfeeding,317  disrupted appetite regulation,318  weight-gain promoting medications,319,320  food selectivity and sensitivity issues,321  behavioral disorders,322  physical activity limitations,323  and use of food rewards.316  A lack of adaptive physical education or sports,324  and specialized supervision and instruction324  also play a role in increasing obesity risk.

Furthermore, it is important to consider that children with disabilities are at a disadvantage when it comes to obesity treatment strategies that are tailored to their needs. For example, most community or school weight management, nutrition or physical activity interventions are not readily adapted for children with disabilities. Therefore, many children with disabilities do not have the support or strategies that they need to address excess weight. Finally, children may face bullying or stigmatization and bias in school. They may also receive unhealthy incentives as rewards from caregivers increasing their risk for obesity. These systemic trends and biases make providing adequate care for children with disabilities extremely difficult.

D.4.b.2 Children With Autism Spectrum Disorder

Children and youth with autism spectrum disorder (ASD) have a higher risk of developing overweight or obesity. In the United States, children and adolescents 2 to 18 years of age with ASD have a 43.7% greater risk of obesity compared with their counterparts without ASD.325  Although the exact mechanisms through which ASD increases the risk for excess weight gain is unknown, a recent meta-analysis of international studies showed that positive moderators to this association include children of certain races and ethnicities, female biological sex, increased age, and living in the United States.325  This meta-analysis did not control for other risk factors for obesity, however, such as use of antipsychotic medications, food intake challenges, or limited physical activity. Hence, the variable of race could be reflective of a negative SDoH.

Several etiological factors have been postulated to contribute to the association between ASD and obesity, including: genetic variants (eg, 16p11.2 deletion and microdeletion 11p14.1),326,327  prenatal exposure to certain infections or medications,328,329  pre and postnatal exposure to toxins,330,331  maternal diabetes,332  maternal obesity,333  intrauterine growth restriction and preterm birth,334,335  food selectivity,336,337  and physical limitations.338,339 

D.4.b.3 Children With Myelomeningocele

Several studies report increased rates of obesity of children with myelomeningocele,340342  with children having more severe disease tending to have higher BMIs.340  Children and adolescents with myelomeningocele have increased total body fat343  and lower energy expenditure,342  compared with children without myelomeningocele. Risk factors for obesity in this population include limited ambulation, sedentary lifestyle, decreased lean body mass, and reduced resting energy expenditure.344  In addition, children with myelomeningocele may be less likely to have routine weight and height, and primary care providers’ discussions may be lacking with respect to addressing healthy lifestyles.

D.4.c. Attention-Deficit/Hyperactivity Disorder

A systematic review and meta-analysis showed significant association between attention-deficit/hyperactivity disorder (ADHD) and obesity among unmedicated individuals with ADHD—but not among medicated individuals.345  The prevalence of obesity was found to be 40% higher among children and adolescents with ADHD, compared with those without ADHD. This association is not affected by gender or by study setting, country, or quality. Causality between ADHD and obesity could not be inferred from this meta-analysis, because the studies were cross-sectional; however, some prospective studies have shown that ADHD precedes the diagnosis of obesity.346,347 

Some of the known symptoms of ADHD may contribute to weight gain. For example, binge eating, which is a manifestation of impulsivity in individuals with ADHD, may result in increased energy intake. Inattentiveness, another symptom of ADHD, may lead to lack of planning, or of following through on a plan, resulting in missed meals or the consumption of unhealthy meals and snacks.348  Other psychiatric comorbidities that are often associated with ADHD—such as depression, anxiety, and circadian rhythm disturbances—may also be risk factors for obesity.348 

Dopamine plays an important role in some of the addictive behaviors of ADHD and obesity. Functional MRI studies have identified shared neuropsychiatric circuits that are associated with reward, response inhibition, and emotional regulation in obesity, ADHD, and abnormal eating behavior.348 

D.4.d. Weight-Promoting Appetitive Traits

Differences in children’s appetitive traits manifest as early as infancy (for example, suckling behavior) and may become more pronounced when children get exposed to an obesogenic food environment.217  Although the exact reasons why some children have better control of their energy intake is unknown, interaction between genetic predisposition and children’s early environment may explain some of the individual differences in appetitive traits. Parent feeding style, as discussed, has been shown to be of importance.217 

Systematic review and meta-analysis of adult data showed a positive association between eating quickly and higher BMI,349  and in longitudinal studies, faster eating rate was associated with excess weight gain.349  Similarly, 2 cross-sectional pediatric studies have reported a positive association between eating fast and childhood and adolescent obesity.350,351  Eating quickly has been suggested to result in greater energy intake.

A recent American Heart Association policy statement on caregiver influences on young children’s eating behaviors synthesized appetitive traits consistently associated with child adiposity. In addition to more rapid eating pace, these traits include eating in the absence of hunger, high enjoyment of food, low responsiveness to satiety, and low level of restrained eating.352 

D.4.e. Medication Use

Medications within many categories have been associated with weight gain. The magnitude of risk associated with medication use is not fully known; therefore, there is an urgent need for more research in this area as well as mediating strategies. Medications implicated include glucocorticoids, sulfonylureas, insulin, thiazolidinediones, antipsychotics, tricyclic antidepressants, and antiepileptic drugs.353356  In particular, second-generation antipsychotics (ie, risperidone, clozapine, quetiapine, and aripiprazole) can lead to rapid weight gain and comorbidities such as prediabetes, diabetes, and dyslipidemia.357,358 

A recent review discusses the more commonly prescribed medications in children and adolescents with obesity and comorbidities, and offers suggestions on alternative therapeutic agents (Table 3).359 

D.4.f. Depression

Children with obesity are more likely to have anxiety and depressive symptoms compared with their peers of healthy weight. It is not clear whether obesity is a risk factor for these symptoms.360,361  Some earlier research reported bidirectional associations between obesity and depression and anxiety. Limitations of some of the studies included small samples; self-reported data on anthropometry; assessment of symptoms based on self-administered questionnaires; and not controlling for potential confounders, such as family history, neuropsychiatric disorders, and SES. A more recent study showed that obesity was a risk factor for anxiety and depression among children and adolescent after adjusting for SES, neuropsychiatric disorders, and family history of anxiety or depression.362 

The association between obesity and depression and anxiety may be attributable to interactions and shared pathophysiological mechanisms between these conditions.363,364  Some of the shared risk factors include genetic, physiologic, and environmental factors. Obesity is associated with subclinical inflammation and oxidative stress, which have been shown to be important etiological factors for depression, and this has been suggested as possible common link between obesity and depression.363  Other factors that can potentially impact the association between obesity and anxiety and depression include sleep disturbance, unhealthy diet, physical activity, antior bullying of children/or bullying of children.

This evaluation is an important part of COT (see COT section in the Treatment section). As with all chronic diseases, a complete history, review of systems (RoS), and physical examination are important for treatment. Specific elements of both history and physical relating to obesity are of special importance. Evaluation of the patient and family’s readiness to change behavior is critical to effectively help with obesity treatment (see algorithm in Appendix 1).

The early and accurate classification of overweight and obesity and identification of obesity-related comorbidities is fundamental to the provision of timely and appropriate treatment (see the Comorbidities section, below). The routine classification of weight status allows for early recognition of abnormal weight gain. This is particularly important because patients—including children and adolescents—often do not perceive overweight and obesity as a health problem.366  Caregivers, families, pediatricians, other pediatric health care providers, and other health care providers367  can also be slow to recognize abnormal weight status, even in the presence of severe obesity.368,369 

Patients and caregivers identify pediatricians and other PHCPs as trusted and preferred sources of information about weight status,370  starting with discussions of feeding practice in infancy and continuing with evaluation of healthy nutrition and activity into adulthood. Pediatricians and other PHCPs are also uniquely qualified to evaluate patients for overweight, obesity, and related comorbidities.

Routine well-child checks (WCCs) in the medical home are an opportune time for the evaluation of a child or adolescent with overweight and obesity, but this can occur during problem-focused visits as well. When the discussion of weight status is normalized and nonstigmatizing, the family and provider can exit a WCC or other visit with a clear and practical plan to improve health and quality of life. Successfully and sensitively treating overweight and obesity can be highly rewarding for both the family and the pediatrician (or other pediatric health care provider), because families suffering from overweight and obesity often have experienced previous shaming or negative experiences with treatment.28,371 

Shaming of children with regard to their weight may happen at school and even at home in misguided efforts to “motivate” the child to adopt healthier behavior. Overt or subtle and unintended bias in health care leads to adverse health, behavioral, and psychological outcomes.61  In addition, when feeding practices are identified as unhealthy, parents may feel blame. It is important, although challenging, for pediatricians and other PHCPs to communicate support and alliance with children, adolescents, and parents as they diagnose and guide obesity treatment.62 

In the AAP statement on obesity bias, steps to provide supportive and nonbiased behavior include recognition of the complex genetic and environmental influences on obesity. Recommendations include use of neutral words like “BMI” or “excess weight” rather than “fat” or “chubby,” use of people-first language (ie, “a child with high weight” or “a child with obesity” rather than “an overweight child” or “an obese child”), an office set-up that accommodates different body sizes, and a private weighing station.28  Ongoing successful communication of support and empathy during obesity treatment is essential to reduce the effect of weight bias, because families will not continue to seek help if they experience stigma.372,373 

Both a complete medical history and physical examination are necessary to evaluate any patient with a chronic disease. Obesity is no exception and, like other chronic diseases, requires comprehensive evaluation in certain areas of both the history and physical examination, which may require additional time to that which is allocated in a routine visit. The medical history includes the chief complaint, history of the present illness, and family history.

  • The chief complaint is notable for determining whether overweight and obesity is a concern for the patient and family. An open-ended question such as “What concerns, if any, do you have about your child’s growth and health?” can provide a wealth of insight on this issue.

  • The history of the present illness provides a more comprehensive picture of the trajectory of overweight and obesity. Starting with an inquiry about maternal weight gain during pregnancy and prenatal factors that predispose to obesity, and then moving on to childhood and later adolescent factors that predispose to obesity, the pediatrician or other pediatric health care provider can glean valuable information on causes and therefore management for a particular patient’s obesity. These prenatal and postnatal causes are described in detail in the Risk Factors section. Information about the onset of excess weight gain and consistency of weight status over time (including a review of the growth curve and previous weight control attempts) can provide an understanding of what weight status represents for the patient. It can also offer clues as to root causes, necessary diagnostic evaluation, and potential therapeutic targets.

  • The family history focuses on obesity-related comorbidities and potential genetic causes of obesity in addition to other family health problems. A family history of obesity and obesity- related comorbidities may influence both evaluation and treatment. Although shared environment, SDoHs, and stress can contribute to obesity within the same family, a family history of obesity can also provide a clue to genetic susceptibility to obesity—especially if the family history includes severe obesity resulting in metabolic and bariatric surgery or severe obesity present in multiple family members and generations.

  • The medication history should be complete and should include medications associated with weight gain, such as antipsychotics, especially atypical antipsychotics; antidepressants including selective serotonin reuptake inhibitors; steroids; anticonvulsants; antihypertensives; birth control agents, including injected forms; and medications used in diabetes mellitus.

Table 4 summarizes the RoS and provides a valuable framework for investigating a variety of obesity-related conditions.

B.1. Social History

A thorough social history is helpful in the evaluation of the child or adolescent with overweight and obesity. An understanding of family living arrangement will identify resources and barriers that are unique to the patient and their family. Factors such as eating routines and schedules; eating at multiple households; and eating environments, such as family meals, eating at a table, eating with or without screens, are all important elements in assessing contributors to and potential treatment targets for excess weight gain. Determining a family’s relationship with food is also important (eg, Is food a common reward? How is food used in celebrations? Is there pressure for the child to eat?).

Because overweight and obesity tends to cluster in social groups as well as families,374  discussions of neighborhood, school, and friend groups can guide pediatricians, other PHCPs, and families to productive areas for treatment. Social history can heighten an awareness of, and provide insight into, patients who are most exposed to negative SDoHs. Given that inequities exist in obesity risk factors, an SDoH evaluation is important to increase awareness and provide insight in identifying patients who are more vulnerable to obesity. Assessment of SDoHs is also important to contextualize the patient’s and family’s treatment challenges. Standardized tools for use in primary care exist and include the Safe Environment for Every Kid model375  and the Accountable Health Communities Health-Related Social Needs Screening Tool.376 

Being alert to and recognizing SDoHs are the initial steps in trauma-informed care (TIC). ACEs can have a profound impact on health over a lifetime and, as noted, include stressors as diverse as harsh parenting, food insecurity, and parental incarceration. These factors can trigger physiologic abnormalities that increase a patient’s risk for obesity, cancer, and numerous other diseases. TIC is characterized by screening and recognition of these ACEs, responding to them, and working to prevent reexposure to trauma. Initial recognition of the importance of ACEs on health occurred in the field of adult obesity treatment. The importance of TIC and addressing ACEs in pediatric obesity management is ongoing.68,377,378 

B.2. Nutrition and Physical Activity History

Gathering a nutrition history and physical activity history often takes the form of a patient and/or caregiver completing a healthy habits survey before seeing the pediatrician or other pediatric health care provider (Table 5). Electronic health records, waiting room kiosks, and emailed previsit surveys can all be used to help gather this information.

There are many additional tools to assess nutrition and physical activity. These include: 24-hour recalls, electronic and written food diaries, telephone- and text-prompted diaries, and various smartphone applications that track food intake. Pedometers and other wearable activity monitors can assist with physical activity assessment. Pediatricians and other PHCPs may find some of these applications and tools at their disposal.

Cultural dietary habits, limited English proficiency, and limited literacy levels may influence the accuracy of the tool used. In comparison with adults, physical activity assessment is challenging, because children and adolescents are less reliable in performing recall of performed activity.379  And, because of the greater burden of overweight and obesity on people of certain race and ethnicities, these differences should be acknowledged and any limitations should be mitigated. An example of a healthy habit survey can be found at https://mainehealth.org/-/media/lets-go/files/childrens-program/pediatric-family-practices/full-healthcare-toolkit.pdf. Sensitivity to cultural, economic, and literacy barriers is necessary with the nutrition history and physical activity history, as with other assessments. Furthermore, the presence of eating disorders, obsessive-compulsive disorder, and other mental health conditions may preclude the use of certain tools that require intensive tracking.

B.3. Assessments for Behavioral Health and Disordered Eating Concerns

Because rates of behavioral health illnesses are greater in patients with obesity than other patients, it is important for pediatricians and other PHCPs to evaluate the emotional health of children with overweight and obesity.380  A common comorbidity of obesity in children is weight-based bullying and teasing.28,43  If a patient responds affirmatively when asked if they have ever been teased or bullied about their weight, pediatricians and other PHCPs can consider provision of resources (such as those found at stopbullying.gov) to the child and parent as well as local counseling referral.

Various in-office tools can be used to address behavioral health disorders seen in greater prevalence in patients with obesity. Overall behavioral functioning can be assessed through the Pediatric Symptom Checklist’s parent or teen versions.381  Evaluation for depression can be conducted through the teen version of the Patient Health Questionnaire 2- or 9- question version.382  Assessment of anxiety by tests such as the General Anxiety Disorder assessment or the Screen for Child Anxiety Related Disorders assessment.383,384  In addition, ADHD can be assessed by the Vanderbilt ADHD Rating Scales.385,386 

As discussed in the AAP clinical reports, “Preventing Obesity and Eating Disorders in Adolescents”387  and “Identification and Management of Eating Disorders in Children and Adolescents,”388  adolescents with obesity may engage in unhealthy practices to lose weight. These practices include skipping meals, using diet pills or laxatives, and inducing vomiting. Therefore, it is important for pediatricians and other PHCPs to evaluate the adolescent with overweight or obesity for these and other related behaviors, and to examine the growth chart for evidence of more rapid than expected decline in BMI.

As noted in the clinical reports above, pediatricians “should be knowledgeable about the variety of risk factors and early signs and symptoms of eating disorders in both male and female children and adolescents. Pediatricians should evaluate patients for disordered eating and unhealthy weight-control behaviors at annual health supervision visits. Pediatricians should evaluate weight, height, and BMI by using age- and sex-appropriate charts, assess menstrual status in girls, and recognize the changes in vital signs that may signal the presence of an eating disorder.”388  For more information on this evaluation, please see the AAP clinical report.388 

B.3.a. Physical Evaluation

A complete physical examination is necessary in the patient with overweight and obesity because of the disease’s complex and multisystem effects. The 2015 article “Physical Examination Findings Among Children and Adolescents with Obesity: An Evidence-Based Review,” by Armstrong et al provides a thorough explanation of special considerations for patients with or at-risk for weight-related illness.365  Pediatricians and other PHCPs are encouraged to reference this AAP-published review. The physical exam also requires focused attention to certain obesity-related findings related to physical evaluation (Table 6). These include:

  • Vital signs such as heart rate, pulse, and blood pressure should be taken; blood pressure should be measured accurately with an appropriately sized cuff.87 

  • Other important signs: short stature may be a sign of a genetic or endocrinologic cause for overweight and obesity. Flat affect may indicate depression, and anxious mood may indicate anxiety. Attention-seeking may be a signal for underlying distress over overweight and obesity. Syndromic features may also offer indications of the presence of an underlying genetic cause for obesity.

  • Skin examination should be performed to look for intertrigo and hidradenitis suppurativa associated with excess skin folds as well as acanthosis nigricans associated with insulin resistance. Flesh-colored striae may be seen on the abdominal wall and/or thighs as an indication of rapid weight gain. The combination of purplish abdominal striae, slowed linear growth, cervicodorsal fat accumulation, proximal muscle wasting, full facies, and hypertension should prompt evaluation for Cushing syndrome.

  • Examination of the head, ears, eyes, nose, and throat should occur to look for papilledema associated with pseudotumor cerebri, tonsillar hypertrophy associated with sleep apnea and goiter associated with thyroid disease.

  • A cardiopulmonary examination should be performed to look for a spectrum of impairment that can be associated with overweight and obesity. Simple deconditioning may present with tachypnea, dyspnea, or tachycardia. Wheezing may be suggestive of intrinsic or exercise-induced asthma. Tonsillar hypertrophy may be a sign that increases the likelihood of sleep apnea. In more severe obesity, congestive heart failure may present with basilar rales or other signs of more significant cardiac disease.

  • Liver size should be assessed by palpation and auscultation. If present, right upper quadrant tenderness should be noted.

  • Genito-urinary examination should be performed to assess pubertal status and genital appearance looking for signs of endocrine or genetic abnormality. Hypogonadism may be present in certain syndromes associated with obesity or be a result of obesity.389,390  More commonly, biological males with abdominal obesity may have a suprapubic fat pad obscuring the penis, a so-called “vanishing penis,” and need instruction on proper voiding and genital hygiene to avoid development of skin breakdown.

  • Neurologic evaluation may reveal papilledema, as described above, as well as paresthesia.

  • Orthopedic findings associated with obesity include abnormal gait, knee tenderness, pes planus, genu valgum (“knock knees”), genu varum (leg bowing), foot pain, back tenderness, and hip pain. Obesity may also make detection of scoliosis more difficult.

  • Neuromuscular evaluation of obesity, as with the orthopedic evaluation of obesity, includes assessment of bone structure, gait and pain, but also includes assessment for balance, coordination, lower limb muscle strength, flexibility and motor skill proficiency. Patients with obesity frequently experience impairment in these areas. Such limitations can result in further reduction of ability to engage in physical activity.391 

“Readiness to change” refers to a patient’s interest in changing a behavior (Importance) and their belief that they can bring about this change (Confidence). This evaluation is important when discussing healthy nutrition and activity with patients who have BMI in the healthy range; it assumes even greater importance with a patient and family who are struggling with overweight, obesity, or severe obesity where health concerns are elevated. This evaluation of readiness to change is central to deciding how and when to embark on obesity treatment. Motivational interviewing (MI), discussed in the Treatment section, provides a useful framework for evaluating and discussing a patient’s readiness to change.392 

Readiness to change, perceptions of weight status, health challenges, nutrition habits, and access to physical activity are influenced by familial, cultural, and socioeconomic factors. For this reason, understanding these factors is beneficial in forging a productive relationship with children and their families. It is also important to remember that patients and families care about their health and their child’s health regardless of race, ethnicity, and/or SES. Caregivers should be reminded that the presence of overweight or obesity is NOT an indication of poor parenting.

Based on BMI classification—and augmented by findings in the history, physical examination, and patient readiness to change assessments—laboratory evaluation of the patient represents the next important step in evaluation. This laboratory evaluation and its connection to the delineation of more common comorbid illnesses is described in the Comorbidities section. Other laboratory evaluations can be performed as clinically indicated.

Children and adolescents with obesity have increased prevalence of comorbidities, and a greater risk for obesity in adulthood, morbidity, and premature death.36,393395  The risk for obesity-related comorbidities increases with age and severity of obesity and prevalence varies by ethnicity and race.396  For example, there is a higher prevalence of NAFLD in Hispanic children and a lower prevalence in Black children.397,398  AI/AN, Black, and Hispanic youth have higher prevalence of prediabetes and diabetes, compared with white youth.399,400  Pediatricians and other PHCPs need to recognize that the association between ethnicity and race and obesity and related comorbidities in both children and adults likely reflects the impact of epigenetic, social, and environmental factors, such as SDoHs, low SES, exposure to structural racism, neighborhood deprivation, and inadequate built environment in these subpopulations.399,401408 

Obesity and related comorbidities should be evaluated concurrently with an obesity-specific history and review of systems, family and social history, physical examination, and laboratory testing. This evaluation provides pediatricians and other PHCPs with an opportunity to assess for both the etiology and complications of obesity (see the Evaluation section). Pediatricians and other PHCPs need to take into consideration patient-specific factors that may increase the risk for comorbidities. For example, prediabetes and diabetes occur more frequently among children who are 10 years and older, are in early pubertal stages, or have a family history of T2DM.399,400,409 

There is compelling evidence that obesity increases the risk for comorbidities and that weight loss interventions can improve comorbidities.80,396,410  Thus, the recommendations for comorbidity evaluation uses input from the technical report on comorbidities for the prevalence, age, and weight category396  associated with comorbidities, and the technical report on treatment of obesity intervention outcomes on dyslipidemia, prediabetes and diabetes, HTN, and NAFLD.80  Studies on optimal age, frequency, benefits, and harms of evaluating for comorbidities for children with obesity remain limited. To address when to begin evaluation, what tests to obtain, and frequency of testing, input from other clinical practice guidelines was also considered.87,88,90,411,412 

The KASs in this section are limited to comorbidities addressed in the technical reports and/or guidelines from professional organizations or societies. Consensus recommendations are included to cover the breadth of relevant comorbidities associated with pediatric overweight and obesity and to provide context for implementation. Each KAS or consensus recommendation is drawn from the technical reports, an extensive review of the literature, and clinical guidelines or position statements from premier organizations or professional societies in the field. The inclusion criteria for the guidelines and position statements are in Table 7. When there was more than 1 guideline from the same organization or professional society, the most recent guideline was given precedence. Other considerations for inclusion were guidelines supported by a technical report or endorsed by the AAP.

The following section is divided into 3 sections:

  • Overall KASs for Laboratory Evaluation of Obesity-Related Comorbidities for children with overweight and obesity (KASs 33.1);

  • Concurrent Treatment of Obesity and Obesity-Related Comorbidities (KAS 4); and

  • Specific Recommendations for Evaluation for Common Comorbidities (KASs 58) and Guidelines for Other Comorbidities.

Recommendations for reevaluation and initial management of common comorbidities are in Appendix 3.

The 2007 AAP Expert Committee on Child Obesity recommended laboratory evaluation for children with obesity for dyslipidemia, prediabetes, and NAFLD starting at 10 years by obtaining a fasting lipid panel, fasting glucose, alanine transaminase, and aspartate transaminase levels every 2 years.92  For children with overweight, the recommendation was only for a fasting lipid panel unless additional risk factors were present (such as family history of obesity-related diseases, elevated BP, elevated lipid levels, or tobacco use).14  KASs 3 and 3.1 build on the 2007 recommendations—taking into account recent studies, guidelines, and pediatrician and other PHCP behaviors—while balancing the harm versus benefit of evaluation at the individual and population levels.

Children ≥10 Years

To encourage a pragmatic and efficient evaluation strategy, KAS 3 and 3.1 recommend that, for children with obesity, evaluation for lipid abnormalities, abnormal glucose metabolism, and liver dysfunction be obtained at the same time and begin at age 10 years. The expectation is that pediatricians and other PHCPs will find it easier to adhere to recommendations when all tests are obtained at the same time. They may order fasting laboratory tests for the evaluation, because a fasting lipid panel is still the recommended test to evaluate for dyslipidemia for children and adolescents with overweight and obesity (see the dyslipidemia section, below, for additional information).

Children 2–9 Years

For children 2 to 9 years of age with obesity, evaluation for lipid abnormalities may be considered (KAS 3.1). This recommendation aligns with the 2011 National Heart Lung Blood Institute (NHLBI) Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents.86  In population-based studies, lipid abnormalities occur in children younger than 10 years, with higher rates among children with obesity.80,395,417  High triglycerides (TG) and low high-density lipoprotein (HDL) levels (the typical pattern of dyslipidemia that occurs with obesity) have been reported in children with obesity as young as 3 years.395 

As the risk profile for NAFLD and diabetes mellitus in children younger than 10 years is lower (especially in the absence of severe obesity), obtaining tests for abnormal glucose metabolism or liver function is not universally recommended for this population.88,90,415,418 

Detailed and specific recommendations are provided in the following sections on dyslipidemia, prediabetes and diabetes mellitus, and NAFLD.

Children With Overweight

For children 10 years and older with overweight, evaluating for lipid abnormalities is recommended in the absence of additional risk factors (KAS 3).86,412  For evaluation of type 2 diabetes mellitus (T2DM), additional risk factors need to be considered, which include: family history, history of gestational diabetes, signs of insulin resistance (such as acanthosis nigricans), and use of obesogenic psychotropic medication.90,358,419  For NAFLD, additional risk factors include family history of NAFLD, central adiposity, signs of insulin resistance, prediabetes or diabetes mellitus, dyslipidemia, and sleep apnea.88 

Considerations for Testing

Among children with obesity, there is clustering of comorbidities, a higher risk profile for more severe disease and/or progression than may be commonly or previously recognized.396,421423  For example, regardless of the definition used for metabolic syndrome, the prevalence is 0% to 4.7% among children with healthy weight and increases to 14.5% to 35% among children and adolescents with obesity.396  In a cohort of 675 children with NAFLD from 12 clinical centers across the United States, one-third had T2DM or prediabetes,422  2 conditions that have significant morbidity in childhood. Adolescents with severe obesity—who have comparable BMI and metabolic profiles as adults—are more likely to present with advanced liver damage and severe systemic inflammation, suggesting that pediatric NAFLD may be more aggressive.424  Similarly, in T2DM, children have a more rapid rate of progression of islet β cell failure and dysglycemia compared with adults.425427 

Concerns about overtesting and cost are warranted but are balanced by the significant impact of obesity and comorbidities on morbidity and mortality. Almost half (43%) of children and adolescents with obesity have at least 1 abnormal lipid level,417  and 1 in 5 US adolescents have prediabetes,423  which are both precursors for future cardiometabolic disease. Although the prevalence of T2DM in children is low, at approximately 1%, the incidence has increased from 9 in 100 000 in 2002 to 13.8 in 100 000 in 2015, a worrisome annual percentage change of 4.8%.399  NAFLD is considered one of the most common chronic liver diseases in children88,397,398,428  and occurs more frequently in male children, older children, and Hispanic children.397,429 

Finally, although obesity prevalence rates continue to rise, the rate of evaluating for obesity or comorbidities in practice is low—suggesting that any concerns about overtesting are likely to be more theoretical than real.3,394,430432 

See Appendix 3 for information on frequency of testing for comorbidities.

There is substantial evidence to support concurrent treatment of obesity and comorbidities to achieve weight loss, avoid further weight gain, and improve obesity-related comorbidities. The majority of studies reviewed in the technical report on comorbidities396  demonstrate an association between overweight and/or obesity, severity of obesity, and higher prevalence of comorbidities. Studies also report improvement in comorbidities with intensive lifestyle treatment, weight loss medication, and/or bariatric surgery.80,126,438  Specifically, cardiometabolic markers improved significantly in children with obesity who underwent intensive pediatric obesity treatment of 3 to 6 months, which provides an opportunity for clinicians to emphasize health outcomes of lifestyle management.80,410,439  Interventions that meet the intensity or “dose” threshold of 26 hours or more over 2 to 12 months can lead to clinically significant improvements in BMI,79  and decreases in BMI can lead to clinically meaningful improvements in comorbidities.440444 

Guidelines for dyslipidemia, T2DM, NAFLD, and HTN all recommend lifestyle treatment of the primary management of the comorbidity.8688,90,414,415,419,420  Although the specific dietary recommendation may differ slightly (eg, CHILD-1 and 2 for dyslipidemia, low-glycemic diet for prediabetes, limiting sugary beverages for NAFLD, and a Dietary Approaches to Stop Hypertension [DASH] Diet for elevated BP), there is overlap between the dietary recommendations and all comorbidities improve with weight stabilization and reduction.80,410,436 

Children are often seen at least once a year for WCCs, at which the pediatrician or other pediatric health care provider reviews the growth chart, provides anticipatory guidance on growth, feeding, nutrition, sedentary screen time, and participation in physical activity. At a minimum, the WCC can include evaluation for comorbidities for children with overweight and obesity, and anticipatory guidance on risk for comorbidities with increasing BMI or obesity. It may be helpful for pediatricians and other PHCPs to include the diagnosis of obesity to the problem list to heighten awareness and remind providers to address weight concerns at subsequent clinic encounters.445,446  In a large adult study, documentation of an obesity diagnosis on a problem list was independently predictive of at least 5% weight loss.445  To avoid any harmful effects related to potential weight bias and stigma, however, pediatricians and other PHCPs need to be mindful of how this diagnosis is conveyed to the child and/or caregiver.28 

There may also be a potential benefit for improved weight outcomes with comorbidity evaluation. In adult studies, identifying obesity-related comorbidities has been shown to be a motivating factor to address weight concerns.447449  The evidence in pediatrics is, however, sparse and inconsistent.434,450  Adolescents identify a desire for improved health as a primary motivation for change.451  Another study analyzed clinic records of 4000 youth aged 10 to 18 years with overweight or obesity in an academic primary care network and found that youth who were evaluated (n = 2815) with a glycosylated hemoglobin (HbA1c) had a decrease in BMI-z slope per year after the HbA1c test compared with similar peers (n = 2087) who had not been evaluated. Among those who had an HbA1c test, the decline in BMI-z slope per year was greater for youth with HbA1c in the prediabetes-range.434  An earlier study with a similar pediatric clinic population but a smaller sample size (n = 128) did not find a positive effect on BMI change following cholesterol evaluation.450  There is a need for more studies before definitive conclusions can be reached about whether evaluating families for comorbidities increases engagement, adoption of healthy choices, and weight loss or has unintended negative effects.

The following sections provide specific recommendations on initial comorbidity evaluation. Guidance on repeat evaluation and initial comorbidity management may be found in Appendix 3.

C1. Dyslipidemia

Children and adolescents with overweight and obesity have increased prevalence of abnormal lipid levels.396  The combination of hypertriglyceridemia and low high-density lipoprotein (HDL) levels, driven largely by underlying insulin resistance, is the most common type of dyslipidemia seen with overweight and obesity. Children and adolescents with overweight and obesity can also have elevated total cholesterol and low-density lipoprotein (LDL) levels.86  NHANES data from 2011 to 2014 showed that prevalence of abnormal lipid level was 3 times higher among children and adolescents with obesity, compared with those with a healthy BMI (43% vs 14%).417 

Studies indicate that cardiovascular risk factors track from childhood into adult life and that lifestyle treatments can improve outcomes with respect to these risk factors.393,413,452  Being aware of the association of these “silent” cardiovascular comorbidities with overweight and obesity—as well as their persistence into adulthood with potential serious health consequences—obliges pediatricians and other PHCPs to perform laboratory testing, educate patients and families about the long-term risks of cardiovascular disease and provide nutrition and activity counseling.

This KAS is supported by both the 2011 NHLBI Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents and 2018 American Heart Association and American College of Cardiology Guidelines, which recommend evaluation for early risk of atherosclerotic cardiovascular disease and counseling on risk-reduction behaviors in children and adolescents.86,411  Evaluation for dyslipidemia with obesity is recommended for younger children, as well as for children 10 years and older. Although data are limited in young children, 1 population-based study showed that 10% of children with obesity aged 3 to 5 years have elevated TG and low HDL levels.395 

In addition to obesity, other risk factors for dyslipidemia include cigarette use, HTN, diabetes, and a family history of cardiovascular disease in a first- or second-degree relative (≤55 years for males and ≤65 years for females) with a history of myocardial infarction, sudden death, or HTN.86,437  All of these conditions warrant laboratory evaluation and may help guide clinical decisions for assessment of dyslipidemia in younger children. Additionally, awareness of an association of social factors, specifically ACEs, with cardiovascular risk factors is important.455 

C.1.a. Laboratory Tests for Diagnosis of Dyslipidemia

The NHLBI expert panel recommends a fasting lipid panel for evaluation of dyslipidemia for children with overweight and obesity.86  Because dietary fats and carbohydrates (particularly simple sugars) increase serum TG concentrations, 8 to 12 hours of fasting before testing is recommended.456  Given that a combination of high TG and low HDL cholesterol is the most common pattern of dyslipidemia observed in children with overweight and obesity, the recommendation to obtain a fasting lipid panel is important, because nonfasting TG levels will not be accurate.86 

For practical purposes, a nonfasting lipid panel using the non-HDL level may be easier to obtain for routine evaluation in the primary care setting. The non-HDL level is the total cholesterol minus the HDL cholesterol level. If the non-HDL cholesterol level is abnormal (non-HDL ≥145 mg/dL) and/or the HDL level is <40 mg/dL, a fasting lipid panel needs to be obtained for diagnosis.412  The nonfasting lipid panel is recommended for all children 9 to 11 years of age to evaluate for familial hypercholesterolemia.86  Estimates are that approximately 25% of children would be referred for a fasting lipid panel because of elevated non-HDL lipid evaluation.457  Because of the elevated risk of lipid abnormality among youth with overweight and obesity, a fasting lipid panel is recommended. See the implementation guide for additional information.

The cut-off criteria for lipids in the 2011 NHLBI guidelines are the same across different age groups, except for triglycerides, as indicated in Table 8.

See Appendix 3 for information on frequency of laboratory testing and information about initial management of dyslipidemia.

C.2. Prediabetes and Type 2 Diabetes Mellitus

T2DM is now increasingly diagnosed in the pediatric population. Between 2002 and 2015, the incidence of T2DM among 10- to 19-year-olds in the United States increased from 9.0 to 13.8 per 100 000.290,399,458  Based on the 2005 to 2016 NHANES, 1 in 5 adolescents (12–18 years) have prediabetes.423  Although uncommon, T2DM has been diagnosed in children younger than 10 years, some as young as 4 years of age.459,460  For this reason, pediatricians and other PHCPs should consider risk factors and symptoms of altered glucose metabolism in all ages (eg, polydipsia, polyphagia, polyuria, blurred vision, unexplained weight loss).

Because obesity is a strong predictor for developing prediabetes and T2DM,423,461,462  pediatricians and other PHCPs need to have an increased index of suspicion when caring for children with obesity, especially in the presence of other risk factors (Table 9).90,408,414,415,463  Both genetics and SDoHs account for some of the racial and ethnic disparities observed in the incidence of T2DM.401,408 

The pathogenesis of prediabetes and T2DM is a peripheral and hepatic resistance to insulin accompanied by progressive loss of islet cell function. Insulin resistance, when assessed by the homeostatic model assessment of insulin resistance test, varies across weight categories, with highest levels observed among children with severe obesity.396  Some children with T2DM have rapidly progressive disease, which underscores the need for early identification and intensive treatment in collaboration with a pediatric endocrinologist.425 

C.2.a. Laboratory Tests for the Diagnosis of Prediabetes and T2DM

Testing for T2DM should always be performed if there is suspicion of hyperglycemia in a patient with symptoms and signs of hyperglycemia, such as new onset thirst (polydipsia), frequent urination (polyuria) or new onset bedwetting, excessive hunger and eating (polyphagia), blurred vision, unexplained or unexpected weight loss, or fatigue.

Diagnostic tests for prediabetes and T2DM are fasting plasma glucose (FPG), 2-hour plasma glucose after oral glucose tolerance test (OGTT), and HbA1c.90  There are several clinical guidelines that do not recommend one test over the other for evaluation.90,268,415,416,419,420,465  Pediatricians and other PHCPs need to be aware of the strengths and shortfalls of each test and take patient preferences and test accessibility into consideration. In addition, the concordance between all 3 tests is imperfect.416  For instance, the FPG is highly reproducible; the OGTT, which does not fare as well on reproducibility, is effective in identifying dysglycemia. This is a good reason to use the OGTT as a confirmation test if the initial test result is equivocal.466470  The OGTT, however, may not be readily available at some medical settings, requires fasting before the test, lasts at least 2 hours, and includes an unpalatable glucose drink—all of which are factors that can limit its use in pediatric outpatient settings as an evaluation test.

The HbA1c test is easy to obtain as fasting is not required. It provides a measure of chronic hyperglycemia, and use of the test has been shown to increase evaluation for T2DM in primary care settings.471  It is also the recommended test for monitoring prediabetes.90,414416,418,464,472  The sensitivity of HbA1c for diagnosing diabetes is lower in children473  when compared with adults.473,474  Pediatricians and other PHCPs also need to be aware that HbA1c levels can be 0.1% to 0.2% higher in individuals with iron deficiency anemia.475,476 

Fasting insulin is not recommended for diagnosis of prediabetes or T2DM because the levels are highly variable and do not reliably correlate with the level of insulin resistance.268,477 

The cut-off values are similar for pediatric and adult populations, as illustrated in Table 10, above. If the results are unequivocally high and indicative of T2DM, obtaining a second or repeat confirmatory test is not recommended; instead, treatment should be initiated.90,415  Guideline recommendations for tracking glycemic control over time use the HbA1c test; however, the FPG can be substituted using the cut-off criteria in Table 10. See the implementation guide for further discussion on use of OGTT or FBG tests.90,414,415,419,464 

See Appendix 3 for more information on frequency of evaluation and on initial management of prediabetes and T2DM.

C.3. Nonalcoholic Fatty Liver Disease

NAFLD is a chronic liver disease marked by steatosis (fat accumulation), inflammation, and fibrosis. The underlying pathogenesis is insulin resistance, which alters the process of fat oxidation in the liver, increasing oxidative stress and inflammation—with resultant liver damage. Among children with obesity, rates as high as 34% have been reported.429 

Three diagnostic terms are used to describe the histology of the disease progression: NAFLD, nonalcoholic fatty liver (NAFL), and nonalcoholic steatohepatitis (NASH). NAFLD refers to the whole spectrum of the disorder, from mild steatosis to cirrhosis of the liver. NAFLD is divided into steatosis (NAFL) and steatohepatitis (NASH). In NAFL, the milder form of the condition, there is fatty infiltration in ≥5% of the liver, with or without fibrosis. In NASH, there is inflammation, steatosis, and fibrosis with ballooning injury to the hepatocytes.433 

The risk profile and natural history of the disorder in the pediatric population are still evolving, given that there are limited long-term studies in children. Pediatric NAFLD may reflect the early onset of a chronic disease with a more aggressive course, particularly once NASH has occurred.424,479  Preadolescent children with NAFLD have higher rates of mortality over 20 years, compared with their peers without NAFLD.479  Children with increasing weight gain; higher levels of alanine transaminase (ALT), γ glutamyl transferase (GGT), and cholesterol at baseline; worsening levels of HbA1c; and an incident diagnosis of T2DM are more likely to have severe disease or progression (Table 11).433,479  However, in a recent study of children 8 to 17 years of age with biopsy-confirmed NAFLD who received standardized nutrition and exercise counseling consistent with the 2007 AAP Expert Recommendations at 12-week intervals over 1 to 2 years, about half demonstrated any improvement in resolution of NASH or regression of fibrosis. Among children with borderline or definite NASH, resolution occurred in about one-third. Adolescents were more likely to develop worsening steatosis and less likely to experience any resolution of NASH or regression in fibrosis than younger children.433 

C.3.a. Laboratory Tests for Diagnosis of NAFLD

The 2017 North American Society of Pediatric Gastroenterology, Hepatology and Nutrition (NASPGHAN) clinical practice guidelines recommend ALT as the preferred test for NAFLD.88  ALT is more specific for liver disease than aspartate transaminase (AST), easily accessible at laboratory centers, minimally invasive relative to other testing modalities for NAFLD, and has been used most often in pediatric NAFLD studies. Higher levels of ALT correlate with more advanced liver disease with steatosis and fibrosis; however, a normal ALT does not definitively exclude NAFLD.429  In a population of children older than 10 years with overweight and obesity who were referred from a primary care clinic, an ALT level ≥80 IU/L had a sensitivity of 57% and a specificity of 71% for NASH.481  Elevations in AST and GGT, especially at baseline, can be indicative of severe disease or rapid progression.433,481 

NAFLD is less common in children younger than 10 years. In an autopsy study of 742 children, 3.3% of 5- to 9-year-old children had fatty liver, compared with 11.3% in 10- to 14-year-olds and 17.3% in 15- to 17-year-olds.397  There is a higher risk for NAFLD in young children 2 to 9 years of age who have severe obesity, however.88  Thus, pediatricians and other PHCPs may consider evaluating NAFLD by obtaining an ALT level every 2 years in these children.

See Appendix 3 for more information on the frequency of evaluation for NAFLD and on managing NAFLD.

C.4. Hypertension

The prevalence of HTN among children and adolescents with overweight and obesity ranges from 5% to 30%, with higher prevalence with increasing BMI percentile.396  Children with excess weight also have abnormal diurnal variation in BP. One-third of children with obesity have a decreased nocturnal BP dip, increasing the potential risk for end-organ damage.482  Among children with obesity, additional cardiometabolic risk factors—such as insulin resistance or dyslipidemia—may affect BP, independent of obesity.

Studies indicate that HTN during childhood and adolescence increases the risk for adult HTN and cardiovascular disease.483485  More concerning, studies have shown that, among children with obesity, HTN is associated with vascular changes, increased left ventricular mass, and carotid intima media thickness during childhood.486,487  These findings support the importance of evaluating for HTN early and consistently throughout childhood and adolescence among individuals with overweight and obesity.413,488 

C.4.a. Evaluation for HTN

Obesity is the strongest risk factor for HTN in childhood.87,488  Elevated BP is observed in early childhood and prevalence increases with age and BMI category.396  A large study conducted in primary care settings found that 8% of children 3 to 5 years of age with obesity had elevated BP levels; the percentage increased to 20% among children 11 to 15 years of age.489  HTN prevalence varies by race and ethnicity, with highest prevalence occurring among non-Hispanic Black and Hispanic youth.490  SES is also a risk factor for HTN,491  as are adverse childhood experiences, both prenatally and during childhood.87  These factors may contribute to the higher prevalence of hypertension observed among non-Hispanic Black and Hispanic youth.490 

Pediatricians and other PHCPs should obtain a history of salt intake (eg, addition of salt while cooking and/or at meals) and sources of sodium from processed, frozen, and fast foods, because high sodium intake is associated with childhood HTN. Obtaining a history of physical activity and inactivity levels is also recommended, because decreased activity levels are associated with childhood HTN.87  Finally, evaluation of sleep duration and disordered breathing are recommended because of the association between abnormal sleep duration and OSA and elevated BP.492,493 

This KAS aligns with the 2017 AAP’s “Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and Adolescents,” which recommends evaluation of elevated BP and HTN for children with obesity at every clinic visit beginning at 3 years of age.87  Frequent monitoring of BP among children with overweight and obesity fosters earlier detection of elevated BP.

C.4.b. Diagnosis of HTN

In 2017, the AAP published a CPG on HTN that included recommendations for evaluation for elevated BP and updated HTN definitions of “elevation,” “stage 1 BP,” and “stage 2 BP” (see Table 12). This CPG recommended that an elevated initial BP measurement (≥90th percentile), taken either by oscillometry or auscultation, should be repeated twice with auscultation and averaged, at the same visit, to determine accurate BP measurement and category. For diagnosis, BP by auscultation should be repeated with confirmed elevated BP measurements on 3 separate clinic visits for elevated BP and stage 1 HTN, and on 2 separate visits for stage 2 HTN.87 

BP measurements should be taken with an appropriately sized cuff; the bladder length should be 80% to 100% of the circumference of the arm, and the width should be at least 40% of the arm circumference.87  (See https://www.cdc.gov/nchs/data/nhanes/nhanes_07_08/manual_an.pdf.)

For children and adolescents with excess weight, a larger cuff size may be required to obtain accurate measurements. For children and adolescents with severe obesity, a thigh cuff may be needed. Additionally, for children and adolescents with obesity, ambulatory blood pressure monitoring (ABPM) is recommended to assess HTN severity and identify possible abnormal circadian BP patterns, which increases risk for end-organ damage. ABPM also helps to identify masked HTN and/or “white coat” HTN.87 

Elevated BP in the office setting is unrecognized in approximately 25% of cases.495  The AAP’s CPG on HTN provides pediatricians and other PHCPs with practical tools to assist with identification of elevated BP and HTN. Improved identification of children at high risk and youth allows for a thorough evaluation, treatment, and follow-up, with the goal of decreasing long-term cardiovascular morbidity and mortality.

See Appendix 3 for more information on repeat evaluation for HTN and on management of HTN. Table 13 lists the KASs for the comorbidities covered in the TR.

D.1. Obstructive Sleep Apnea

OSA is a sleep disorder “characterized by prolonged partial upper airway obstruction and/or intermittent complete obstruction that disrupts normal ventilation during sleep.”89  The condition is associated with cardiovascular complications, neurocognitive impairment, and decreased quality of life. Children with obesity have a higher prevalence of OSA: 45% among children obesity compared with 9% among children with healthy weight. One study indicated that a 1-unit increase in the BMI SD score increased the odds of having OSA by a factor of 1.9 independent of age, sex, tonsillar hypertrophy, and asthma.441 

Evaluation for OSA is based on history of symptoms and examination. Children with obesity, tonsillar hypertrophy, craniofacial anomalies, trisomy 21, and neuromuscular disorders are at higher risk for OSA. Common symptoms include frequent snoring, gasps or labored breathing during sleep, disturbed sleep, daytime sleepiness, inattention and/or learning problems, nocturnal enuresis, and headaches. Examination findings may include tonsillar hypertrophy, adenoidal facies, micro- or retrognathia, high-arched palate, and elevated BP. Diagnosis is made by obtaining a polysomnography, the gold standard test, with an apnea-hypopnea index of 1 or more episodes per hour in children.496  Because of limited availability of sleep centers with pediatric expertise, referral to a pediatric otolaryngologist for further evaluation, diagnosis, and management may be needed.

The CPG authors recommend pediatricians and other PHCPs obtain:

  • A sleep history, including symptoms of snoring, daytime somnolence, nocturnal enuresis, morning headaches, and inattention, among children and adolescents with obesity to evaluate for OSA.

  • A polysomnogram for children and adolescents with obesity and at least 1 symptom of disordered breathing.

See Appendix 3 for more information on the initial management of OSA.

Polycystic ovarian syndrome (PCOS) is a heterogeneous disorder characterized by hyperandrogenism and disordered ovulatory function and is often associated with obesity and insulin resistance. The condition increases risk for infertility, T2DM, cardiovascular disease, and cancer.497 

Four different sets of criteria have been published for diagnosis of PCOS in adults as outlined by differing professional organizations (Table 14).498  Establishment of diagnostic criteria for PCOS in adolescence has been difficult, because characteristic features of PCOS can be normal physiologic events during early adolescence.499  International pediatric and adolescent specialty societies have made recommendations for diagnosis specific to adolescents, which include the following: (1) evidence of clinical or biochemical hyperandrogenism, and (2) persistent irregular menstrual cycles (<20 days or >45 days) 2 years after menarche.500  Limited data are available on prevalence of PCOS in adolescents. Estimates range from 3% to 11%, depending on the criteria for diagnosis.501 

Evaluation for PCOS in an adolescent requires first excluding other medical conditions that may cause menstrual dysfunction (oligomenorrhea or amenorrhea) and/or signs of androgen excess (acne, hirsutism, or alopecia). Additionally, for adolescents, evaluation should occur 2 years after menarche, because irregular menstrual cycles are not uncommon during this timeframe. Laboratory testing may include: 17-hydroxyprogesterone, total testosterone, free testosterone, sex hormone-binding globulin, dehydroepiandrosterone sulfate, androstenedione, luteinizing hormone, follicle-stimulating hormone, estradiol, prolactin, free thyroxine, thyroid stimulating hormone, and insulin. Interpretation of laboratory results should be made in the context of age-appropriate reference ranges; therefore, referral to a laboratory that can perform ultrasensitive pediatric assays is recommended. Routine ovarian imaging is not indicated for the diagnosis of PCOS in adolescents.498,502  An algorithm for evaluation is provided in the implementation materials from previously published consensus recommendations.503 

See Appendix 3 for more information on the initial management of PCOS.

The CPG authors recommend pediatricians and other PHCPs:

  • Evaluate for menstrual irregularities and signs of hyperandrogenism (ie, hirsutism, acne) among female adolescents with obesity to assess risk for PCOS.

D4. Depression

The relationship between pediatric obesity and depression is less well understood than the physical comorbidities; however, identification of depression is an important component of the assessment and management of pediatric obesity, given its potential impact on treatment outcomes. A systematic review and meta-analyses conducted in 2019 showed that children 18 years and younger with obesity have a 32% increased odds of having or developing depression compared with children of healthy weight, with the highest odds (44%) among females with obesity.504 

Studies are limited on the effect of treatment of pediatric obesity on depression. A recent meta-analysis of 36 studies found a small but significant reduction in depressive symptoms following structured pediatric obesity treatment. Notably, no adverse mental health outcomes were reported.505  Additionally, the interventions technical report indicates that obesity treatment may improve psychosocial outcomes for youth with obesity, including quality of life.80  Further research in this area is needed; however, pediatricians and other PHCPs should be aware that obesity treatment interventions have not been associated with increased symptoms of depression.80 

Evaluation for depression includes awareness of symptoms and risk factors. Symptoms include irritability, fatigue, insomnia, excessive sleeping, decline in academic performance, family conflict, and weight changes. Risk factors include personal or family history of depression, substance use, trauma, frequent psychosomatic complaints, psychosocial stressors, and other mental health conditions. The AAP CPG for depression recommends evaluating adolescents 12 years and older for depression annually using a formal self-report tool, such as the Patient Health Questionnaire-9.506  Additionally, routine monitoring of psychosocial function and using an evaluation tool when a patient presents with symptoms of depression is recommended.

If initial evaluation for depression is positive, evaluation with a standardized depression tool should be conducted. Assessment for depression should also include direct, separate interviews with the patient and family members to include functional impairment at home, school, and peer settings and safety and/or suicide risk.506  The implementation materials include additional information and resources, including tools for pediatricians and other PHCPs, in addition to an assessment and management algorithm.506 

See Appendix 3 for more information on the initial management of depression.

The CPG authors recommend pediatricians and other PHCPs:

  • Monitor for symptoms of depression in children and adolescents with obesity and conduct annual evaluation for depression for adolescents 12 years and older with a formal self-report tool.

D5. Orthopedic Comorbidities

D.5.a. Slipped Capital Femoral Epiphysis

Slipped capital femoral epiphysis (SCFE) is the most common hip disorder in the adolescent period. It occurs between 9 and 16 years of age, spanning periods of rapid linear growth. There is a 1.5:1 male-to-female ratio, and SCFE occurs more often in Black, Hispanic, and AI/AN children.507,508  SCFE is bilateral in 25% to 80% of cases.507  Weakening of the proximal femoral physis (growth plate) causes a slip in the physis, with a corresponding displacement of the epiphysis (femoral head). Risks such as obesity exert mechanical stress on the physis, whereas metabolic conditions (eg, hypothyroidism, hypopituitarism) weaken the physis, creating the ideal setup for a slip.

The common presentation is hip pain, although many children may present with knee pain alone or in addition to hip pain. The pain can happen only with weight bearing or be constant. On physical examination, there is external rotation with passive hip flexion, limitation of internal rotation and antalgic gait. Pain can also be elicited passively with internal rotation of the hip. SCFE is characterized as stable if the child can bear weight with or without crutches and as unstable when weight-bearing is not possible.509  Because SCFE can be bilateral, the pediatrician or other pediatric health care provider needs to remember to obtain a history and exam for the contralateral leg. The history and examination should also exclude differential diagnoses for hip pain (eg, infections, inflammation or autoimmune conditions, neoplasms, and trauma).

As the pathophysiologic process continues, the child is at greater risk for increased morbidity, including avascular necrosis. Thus, the importance of early diagnosis cannot be overemphasized. Once SCFE is suspected, pediatricians and other PHCPs should confirm the diagnosis and place an emergent referral to the orthopedic surgeon. The mainstay for diagnosis is plain radiographs of the hip and pelvis (Table 15). Ultrasonography and computerized tomography are not useful. In cases with equivocal radiography results and a high index of suspicion, MRI, which is more sensitive at assessing the physis, can be obtained.

See Appendix 3 for more information on the initial management of SCFE.

D.5.b. Blount Disease

Blount disease is a growth disorder that primarily affects the proximal medial tibial physis and epiphysis.510,511  It often presents as a triad of asymmetric tibia vara, tibial torsion, and precurvatum. As with SCFE, excess weight is a risk factor, because it increases mechanical stress on the physis. Blount disease disproportionately affects non-Hispanic Black or Hispanic children.510,511  The reason for this predilection is unclear, but it may reflect epigenetic, social, or cultural factors that affect early ambulation, growth, or obesity. Other risk factors include a family history of Blount disease and ambulation before 12 months of age.510,511  Symptoms and signs include leg pain, abnormal gait with bowing of the lower legs, and leg-length discrepancy.

Blount disease is classified into 2 categories: (1) infantile or early-onset, and (2) late-onset or adolescent Blount disease, based whether the onset occurred before or after age 10 years, respectively. Infantile Blount disease is bilateral but asymmetric, occurs more often in males, and often includes a preceding history of early ambulation. For young children, pediatricians and other PHCPs should exclude physiologic bowing typically seen during toddlerhood, which is bilateral but symmetrical and resolves by age 3 or 4 years. In the adolescent subtype, the tibia vara deformity is milder, unilateral, and predominantly associated with severe obesity.510513 

Plain radiographs are the initial imaging of choice (Table 15). When used, MRI provides a more sensitive investigation of the deformity.

See Appendix 3 for more information on the initial management of Blount disease.

The CPG authors recommend pediatricians and other PHCPs:

  • Perform a musculoskeletal review of systems and physical examination (eg, internal hip rotation in growing child, gait) as part of their evaluation for obesity.

  • Recommend immediate and complete activity restriction, nonweight-bearing with use of crutches, and refer to an orthopedic surgeon for emergent evaluation, if SCFE is suspected. PHCPs may consider sending the child to an emergency department if an orthopedic surgeon is not available.

D.5.c. Idiopathic Intracranial Hypertension

Idiopathic intracranial hypertension (IIH) (previously known as pseudotumor cerebri) is a neurologic condition with serious long-term morbidity.514,515  It occurs most often in females of child-bearing age, and obesity is a well-established risk factor.516518  In a population-based study in Olmstead County, Minnesota, the incidence of IIH among adult females aged 15 to 44 years with obesity was 3.5-fold higher than that of all females in that age group.517 

The pathogenesis is unclear, hence the name; however, 3 hypothesized mechanisms are increased venous pressure, decreased cerebrospinal fluid (CSF) drainage, and increased CSF production. Other factors associated with for IIH include medications (eg, doxycycline, tetracyclines, retinoic acid, sulfonamides), autoimmune disorders (eg, systemic lupus erythematosus), and hormonal disorders (eg, Cushing disease, Addison disease). A higher prevalence of IIH has also been reported in females with PCOS.519 

Typical symptoms are persistent headaches, pulsatile synchronous tinnitus, and visual changes or loss, although the history can be variable. Physical examination includes a fundoscopy for papilledema and a thorough neurologic evaluation for cranial nerve deficits such as sixth nerve palsy. The presence of altered consciousness or neurologic deficit with localized peripheral findings should prompt pediatricians and other PHCPs to consider another etiology. The serious sequelae for IIH is vision loss. Thus, a review of system should be obtained to evaluate any child with obesity who has significant or progressive headaches. There should also be a high index of suspicion for IIH with new-onset headaches and significant weight gain (5% to 15% of body weight), particularly when it occurs in the prior 12 to 18 months.518,520 

Initial evaluation for IIH involves conducting comprehensive evaluation by the neurologist and ophthalmologist or at an integrated IIH clinic.

See Appendix 3 for more information on the initial management of IIH.

The CPG authors recommend pediatricians and other PHCPs:

  • Maintain a high index of suspicion for IIH with new- onset or progressive headaches in the context of significant weight gain, especially for females.

In summary, a thorough history and physical examination is invaluable in guiding pediatricians’ and other PHCPs’ assessment for comorbidities. This section of the CPG, the algorithm in Appendix 1, Appendix 3, and the accompanying implementation resources provide a framework for evaluation, reevaluation, and initial management. Obesity is a linchpin disorder with attendant comorbidities, some of which are not covered in this section or in the technical report (eg, pes planus). For these comorbidities, pediatricians and other PHCPs are encouraged to seek resources available through the AAP and other professional societies.

Obesity is a chronic disease and should be treated with intensive and long-term care strategies, provision of ongoing medical monitoring and treatment of associated comorbidities and ongoing access to obesity treatment. As noted previously, obesity is associated with increased prevalence of comorbidities, including abnormal lipids, glucose dysregulation and other endocrinopathies, abnormal liver enzymes, and elevated BP. A key component of treating obesity is to concurrently monitor and treat the comorbidities (see Comorbidities section).

The chronic care model requires care to be delivered within the context of individual patient factors, taking into consideration the child’s household and familial influences, access to healthy food and activity spaces, and other SDoHs.522  Recommendations for obesity treatment should be integrated within existing community and social systems.521  The medical home model is the preferred standard of care for children who have chronic conditions,522  and the child’s medical home should serve as a care coordinator in the treatment of children with obesity, coordinating with subspecialists, including obesity treatment specialists, and community resources.

Treatment of obesity varies based on individual-level factors. No specific studies were found that compare different treatments by a patient’s underlying condition, special needs, or developmental status. Nonetheless, it is important to recognize that the following recommendations will require adaptation based on the patient’s unique medical, family, developmental, social, and environmental factors. No evidence exists, however, to exclude children with special health care needs, complex disease, or developmental limitations from the treatment options outlined below, except where specifically noted.

The evidence for pediatric obesity treatment that is presented in this CPG shows that several treatments are effective in treating both obesity and related comorbidities. It is important to note, however, that in all of these studies, if the treatment is discontinued, children tend to regain weight and lose the attendant health benefits. There is limited longitudinal evidence about durability of weight change after treatment. The natural course of obesity across the lifespan is characterized by responses to treatment and relapse when treatment ends.77  Therefore, continuous coordinated care is required to support ongoing obesity treatment throughout childhood and adolescence into young adulthood.503 

In the field of pediatric nutrition, in the treatment of both obesity and eating disorders, concerns have been raised as to whether diagnosis and treatment of obesity may inadvertently place excess attention on eating habits, body shape, and body size and lead to disordered eating patterns as children grow into adulthood. The literature refutes this relationship, however. Cardel et al refer to multiple studies that have demonstrated that, although obesity and self-guided dieting consistently place children at high risk for weight fluctuation and disordered eating patterns, participation in structured, supervised weight management programs decreases current and future eating disorder symptoms (including bulimic symptoms, emotional eating, binge eating, and drive for thinness) up to 6 years after treatment.378,505,523  The structure and underlying principles of the primary care-based and intensive health behavior and lifestyle programs described here share multiple similarities with eating disorder programs. These include a focus on increasing healthful food consumption, participating in physical activity for enjoyment and self-care reasons, and improving overall self-esteem and self-concept. Structured and professionally run pediatric obesity treatment is associated with reduced eating disorder prevalence, risk, and symptoms.505,523 

MI (also discussed in the Evaluation section) is a patient-centered counseling style that identifies and reinforces a patient’s own motivation for change—in contrast to the more traditional approach in which a provider prescribes behavior change. MI guides families to identify a behavior to change, based on what the parent(s) or child feels is important and can be accomplished.524 

MI does not impose a particular goal but is successful