Childhood and adolescent obesity is a multifaceted and widespread health issue that often persists over time. It is characterized by a BMI equal to or greater than the 95th percentile for age and gender in children aged two years and older. In cases of severe obesity, the BMI threshold is equal to or greater than the 120th percentile.
For younger children, the Centers for Disease Control (CDC) recommend utilizing age, gender, and weight-for-length charts provided by the World Health Organization, instead of relying on BMI. In the United States, the prevalence of obesity in children has increased more than threefold since the 1960s, with rates tending to rise with age. Failing to prevent, identify, and address childhood obesity leads to concurrent health issues in children that often persist into adulthood.
Epidemiology
Between 1963 -2000, there was a significant rise in the prevalence of obesity among children aged 6 to 11, increasing from 4.2% to 15.3%. The rate of obesity is even higher among adolescents, with 20.6% of 12 to 19-year-olds being affected. In the United States, approximately 13.5 million adolescents struggle with obesity.
There are notable disparities in obesity rates across different racial and ethnic groups, with non-Hispanic Black and Mexican American children exhibiting higher rates than non-Hispanic White children.
Factors contributing to these disparities include the educational level and income of parents, limited access to healthy food options, and a lack of safe opportunities for physical activity. Furthermore, children with disabilities such as autism and intellectual disabilities face an increased risk of developing obesity.
Anatomy
Pathophysiology
Neuroendocrine feedback mechanisms play a crucial role in regulating appetite and satiety. Various gastrointestinal hormones, such as ghrelin, stimulate appetite, while hormones like GLP-1, Peptide YY, CCK, and vagal neural feedback inhibit appetite and promote feelings of satiety. Adipose tissue also provides feedback on energy stores through hormones like adiponectin and leptin, which act as satiety signals.
These hormones relay feedback to the arcuate nucleus in the hypothalamus, which, in turn, sends behavioral and autonomic signals to the solitary tract nucleus in the brainstem, leading to the secretion of gastrointestinal hormones. Neuropeptides in the brain, including PYY, AgRP, and orexin, stimulate appetite, whereas melanocortin and alpha-melanocyte-stimulating hormones promote satiety. Genetic deficiencies in MCR4 have been associated with increased food-seeking behavior.
Insufficient sleep has been linked to decreased levels of circulating leptin, increased levels of ghrelin, and heightened self-reported hunger. The interaction between the gut, adipose tissue, and brain maintains a delicate balance between appetite stimulation and adiposity. Mutations in genes involved in the secretion of these hormones have attracted interest in terms of epigenetic modifications and their potential as therapeutic targets.
Etiology
The development of obesity is influenced by a array of factors, making its etiology complex and multifaceted. Genetic, biological, environmental, socioeconomic, and cultural factors all contribute to the onset of obesity. While genetics and biology are predetermined, the other factors can be modified through interventions. These include the eating, sleeping, and exercise behaviors within a family, the availability of nutritious food options in schools and communities, access to safe environments for physical activity, and the impact of adverse childhood experiences.
When calorie intake exceeds energy expenditure, weight gain occurs, eventually leading to obesity. Although genetic factors play a role, they influence less than other factors. Changes in food preferences over the past few decades, driven by marketing strategies and the increased availability of high calorie processed foods such as fast food and sugary beverages, have contributed to the rise in obesity rates.
Consumption of these energy-dense foods, larger portion sizes, and increased snacking have been strongly associated with the significant increase in obesity in developed nations. Additionally, reduced levels of physical activity and increased sedentary behaviors, such as prolonged screen time from smartphones, computers, televisions, and video games, have contributed to the obesity problem. Cultural factors influence feeding patterns and food choices, and children often model their eating behaviors after their parents and families from a very young age.
Research shows that higher parental education and the establishment of structured family meals have a positive impact on children’s healthy food choices. Factors such as families eating together, exposing children to a variety of nutritious food options, and avoiding distractions like television during meals create a supportive food environment that reduces the risk of obesity development. Several additional risk factors have been identified that can predispose individuals to obesity.
Perinatal and postnatal conditions such as elevated maternal BMI during pregnancy, high birth weight, rapid weight gain during infancy and early childhood, and breastfeeding versus formula feeding can all impact obesity risk. Environmental chemicals, the composition of gut microbiota, early use of antibiotics, and adverse life experiences are also being explored as potential risk factors for obesity.
Genetics
Prognostic Factors
Timely identification and intervention in cases of obesity are essential for reducing associated health complications and improving long-term outcomes. As the burden of complications tends to escalate with age and severity, early diagnosis and treatment provide the most significant opportunity for maintaining good health.
When lifestyle modifications and behavioral interventions prove ineffective, healthcare professionals should promptly refer patients for pharmacological and surgical interventions. Failing to provide appropriate treatment can result in children with obesity transitioning into adulthood with obesity, putting them at risk for enduring negative health consequences.
Clinical History
Clinical History
The examiner should confront if the family has concerns regarding the child’s growth and weight and why. Prenatal factors such as gestational diabetes or maternal weight gain during pregnancy should be reviewed as they may increase the likelihood of obesity. Birth and perinatal history should be assessed, including information about intrauterine growth retardation followed by rapid catch-up growth or having a baby with a large size for gestational age.
Exploring meal composition, feeding patterns, snacking habits, and screen time can help identify potential causes of disproportionate weight gain. Assessing the type and duration of physical activity undertaken by the child. Analyzing the weight and height growth charts for any sudden changes in height, weight, and BMI trajectories may indicate underlying factors. Certain genetic conditions may present with excessive appetite and food-seeking conducts.
Genetic susceptibility might be considered if family members have undergone bariatric surgery for severe obesity or if obesity is observed across multiple generations. The presence of hypertension, diabetes, or cardiovascular disease in family members also increases the child’s risk of developing similar conditions. Parental obesity is a significant risk factor, likely influenced by genetics and social determinants of health. Clinicians should help families understand that childhood obesity increases the likelihood of developing several chronic diseases.
If there is a history of significant head trauma preceding sudden weight gain, a hypothalamic cause may be suspected. Symptoms such as easy bruising, muscle weakness, fatigue, and central obesity may indicate Cushing syndrome. Dry skin, cold intolerance, and anterior neck swelling may suggest hypothyroidism. However, it is important to note that less than 1% of children with obesity will be diagnosed with an endocrine cause, despite some families attributing weight gain to hormone imbalances. Additionally, a review of medications associated with obesity, such as steroids, antipsychotics (e.g., risperidone), and antiepileptics (e.g., valproate), can help identify drug-induced obesity.
Physical Examination
Physical Examination
The physical examination should include calculating the BMI, and accurate BP measurement using an appropriately sized cuff is essential. A comprehensive head-to-toe examination should follow to identify potential causes and complications of obesity.
Facial and body dysmorphisms can provide clues to genetic disorders. Instances include hypogonadism, almond-shaped eyes, short neck, small hands and feet indicative of Prader-Willi syndrome, hypotonia, upward slanting eyes, and transverse palmar creases indicative of Down syndrome, as well as central obesity, round face, and more fatty tissue between the shoulders.
Cognitive impairment may suggest the presence of a genetic syndrome. Short stature may be associated with Albright hereditary osteodystrophy or hormone deficiencies. A specialist should further evaluate eye findings such as papilledema (indicating pseudotumor cerebri), nystagmus, and retinal degeneration (associated with Bardet-Biedl syndrome).
Skin changes such as acanthosis nigricans, acne, and hirsutism may indicate insulin resistance or polycystic ovary syndrome. Assessing sexual maturity can help identify premature adrenarche in obese girls. Dyspnea and wheezing may indicate asthma, hepatomegaly, and abdominal tenderness, suggesting non-alcoholic fatty liver disease. Knee and Hip mobility restrictions may be signs of slipped capital femoral epiphysis and Blount disease.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnoses
Hypothyroidism
Growth Hormone Deficiency
Cushing Syndrome
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
The management of pediatric obesity focuses on treating obesity itself and its associated comorbidities, aiming for weight loss, prevention of further weight gain, and improvement of complications. Behavioral change is fundamental in this approach. Family-based interventions play a crucial role in reducing BMI. T
hese interventions include limiting the consumption of sweetened beverages and fast food, increasing the intake of fruits and vegetables, and promoting increased physical activity. While there is no sufficient evidence to support the use of weight loss medications as a standalone therapy in pediatric patients, they are recommended as adjuncts when intensive behavioral interventions alone have not been successful.
It should be noted that many medications commonly used in adults have not received FDA approval for use in children, and further research is ongoing in this area. However, orlistat is an FDA-approved medication for children aged 12 years and older with obesity. In rare genetic conditions such as proopiomelanocortin and leptin deficiency, melanocortin 4 receptor agonists like setmelanotide have received FDA approval for children aged six and older.
Continued research and evaluation of pharmacological treatments for pediatric obesity are necessary to expand the available options and ensure their safety and effectiveness in this population. The focus remains on a comprehensive approach that combines behavioral interventions, lifestyle modifications, and when appropriate, pharmacological interventions to address the complex nature of pediatric obesity.
Childhood and adolescent obesity is a multifaceted and widespread health issue that often persists over time. It is characterized by a BMI equal to or greater than the 95th percentile for age and gender in children aged two years and older. In cases of severe obesity, the BMI threshold is equal to or greater than the 120th percentile.
For younger children, the Centers for Disease Control (CDC) recommend utilizing age, gender, and weight-for-length charts provided by the World Health Organization, instead of relying on BMI. In the United States, the prevalence of obesity in children has increased more than threefold since the 1960s, with rates tending to rise with age. Failing to prevent, identify, and address childhood obesity leads to concurrent health issues in children that often persist into adulthood.
Between 1963 -2000, there was a significant rise in the prevalence of obesity among children aged 6 to 11, increasing from 4.2% to 15.3%. The rate of obesity is even higher among adolescents, with 20.6% of 12 to 19-year-olds being affected. In the United States, approximately 13.5 million adolescents struggle with obesity.
There are notable disparities in obesity rates across different racial and ethnic groups, with non-Hispanic Black and Mexican American children exhibiting higher rates than non-Hispanic White children.
Factors contributing to these disparities include the educational level and income of parents, limited access to healthy food options, and a lack of safe opportunities for physical activity. Furthermore, children with disabilities such as autism and intellectual disabilities face an increased risk of developing obesity.
Neuroendocrine feedback mechanisms play a crucial role in regulating appetite and satiety. Various gastrointestinal hormones, such as ghrelin, stimulate appetite, while hormones like GLP-1, Peptide YY, CCK, and vagal neural feedback inhibit appetite and promote feelings of satiety. Adipose tissue also provides feedback on energy stores through hormones like adiponectin and leptin, which act as satiety signals.
These hormones relay feedback to the arcuate nucleus in the hypothalamus, which, in turn, sends behavioral and autonomic signals to the solitary tract nucleus in the brainstem, leading to the secretion of gastrointestinal hormones. Neuropeptides in the brain, including PYY, AgRP, and orexin, stimulate appetite, whereas melanocortin and alpha-melanocyte-stimulating hormones promote satiety. Genetic deficiencies in MCR4 have been associated with increased food-seeking behavior.
Insufficient sleep has been linked to decreased levels of circulating leptin, increased levels of ghrelin, and heightened self-reported hunger. The interaction between the gut, adipose tissue, and brain maintains a delicate balance between appetite stimulation and adiposity. Mutations in genes involved in the secretion of these hormones have attracted interest in terms of epigenetic modifications and their potential as therapeutic targets.
The development of obesity is influenced by a array of factors, making its etiology complex and multifaceted. Genetic, biological, environmental, socioeconomic, and cultural factors all contribute to the onset of obesity. While genetics and biology are predetermined, the other factors can be modified through interventions. These include the eating, sleeping, and exercise behaviors within a family, the availability of nutritious food options in schools and communities, access to safe environments for physical activity, and the impact of adverse childhood experiences.
When calorie intake exceeds energy expenditure, weight gain occurs, eventually leading to obesity. Although genetic factors play a role, they influence less than other factors. Changes in food preferences over the past few decades, driven by marketing strategies and the increased availability of high calorie processed foods such as fast food and sugary beverages, have contributed to the rise in obesity rates.
Consumption of these energy-dense foods, larger portion sizes, and increased snacking have been strongly associated with the significant increase in obesity in developed nations. Additionally, reduced levels of physical activity and increased sedentary behaviors, such as prolonged screen time from smartphones, computers, televisions, and video games, have contributed to the obesity problem. Cultural factors influence feeding patterns and food choices, and children often model their eating behaviors after their parents and families from a very young age.
Research shows that higher parental education and the establishment of structured family meals have a positive impact on children’s healthy food choices. Factors such as families eating together, exposing children to a variety of nutritious food options, and avoiding distractions like television during meals create a supportive food environment that reduces the risk of obesity development. Several additional risk factors have been identified that can predispose individuals to obesity.
Perinatal and postnatal conditions such as elevated maternal BMI during pregnancy, high birth weight, rapid weight gain during infancy and early childhood, and breastfeeding versus formula feeding can all impact obesity risk. Environmental chemicals, the composition of gut microbiota, early use of antibiotics, and adverse life experiences are also being explored as potential risk factors for obesity.
Timely identification and intervention in cases of obesity are essential for reducing associated health complications and improving long-term outcomes. As the burden of complications tends to escalate with age and severity, early diagnosis and treatment provide the most significant opportunity for maintaining good health.
When lifestyle modifications and behavioral interventions prove ineffective, healthcare professionals should promptly refer patients for pharmacological and surgical interventions. Failing to provide appropriate treatment can result in children with obesity transitioning into adulthood with obesity, putting them at risk for enduring negative health consequences.
Clinical History
The examiner should confront if the family has concerns regarding the child’s growth and weight and why. Prenatal factors such as gestational diabetes or maternal weight gain during pregnancy should be reviewed as they may increase the likelihood of obesity. Birth and perinatal history should be assessed, including information about intrauterine growth retardation followed by rapid catch-up growth or having a baby with a large size for gestational age.
Exploring meal composition, feeding patterns, snacking habits, and screen time can help identify potential causes of disproportionate weight gain. Assessing the type and duration of physical activity undertaken by the child. Analyzing the weight and height growth charts for any sudden changes in height, weight, and BMI trajectories may indicate underlying factors. Certain genetic conditions may present with excessive appetite and food-seeking conducts.
Genetic susceptibility might be considered if family members have undergone bariatric surgery for severe obesity or if obesity is observed across multiple generations. The presence of hypertension, diabetes, or cardiovascular disease in family members also increases the child’s risk of developing similar conditions. Parental obesity is a significant risk factor, likely influenced by genetics and social determinants of health. Clinicians should help families understand that childhood obesity increases the likelihood of developing several chronic diseases.
If there is a history of significant head trauma preceding sudden weight gain, a hypothalamic cause may be suspected. Symptoms such as easy bruising, muscle weakness, fatigue, and central obesity may indicate Cushing syndrome. Dry skin, cold intolerance, and anterior neck swelling may suggest hypothyroidism. However, it is important to note that less than 1% of children with obesity will be diagnosed with an endocrine cause, despite some families attributing weight gain to hormone imbalances. Additionally, a review of medications associated with obesity, such as steroids, antipsychotics (e.g., risperidone), and antiepileptics (e.g., valproate), can help identify drug-induced obesity.
Physical Examination
The physical examination should include calculating the BMI, and accurate BP measurement using an appropriately sized cuff is essential. A comprehensive head-to-toe examination should follow to identify potential causes and complications of obesity.
Facial and body dysmorphisms can provide clues to genetic disorders. Instances include hypogonadism, almond-shaped eyes, short neck, small hands and feet indicative of Prader-Willi syndrome, hypotonia, upward slanting eyes, and transverse palmar creases indicative of Down syndrome, as well as central obesity, round face, and more fatty tissue between the shoulders.
Cognitive impairment may suggest the presence of a genetic syndrome. Short stature may be associated with Albright hereditary osteodystrophy or hormone deficiencies. A specialist should further evaluate eye findings such as papilledema (indicating pseudotumor cerebri), nystagmus, and retinal degeneration (associated with Bardet-Biedl syndrome).
Skin changes such as acanthosis nigricans, acne, and hirsutism may indicate insulin resistance or polycystic ovary syndrome. Assessing sexual maturity can help identify premature adrenarche in obese girls. Dyspnea and wheezing may indicate asthma, hepatomegaly, and abdominal tenderness, suggesting non-alcoholic fatty liver disease. Knee and Hip mobility restrictions may be signs of slipped capital femoral epiphysis and Blount disease.
Differential Diagnoses
Hypothyroidism
Growth Hormone Deficiency
Cushing Syndrome
The management of pediatric obesity focuses on treating obesity itself and its associated comorbidities, aiming for weight loss, prevention of further weight gain, and improvement of complications. Behavioral change is fundamental in this approach. Family-based interventions play a crucial role in reducing BMI. T
hese interventions include limiting the consumption of sweetened beverages and fast food, increasing the intake of fruits and vegetables, and promoting increased physical activity. While there is no sufficient evidence to support the use of weight loss medications as a standalone therapy in pediatric patients, they are recommended as adjuncts when intensive behavioral interventions alone have not been successful.
It should be noted that many medications commonly used in adults have not received FDA approval for use in children, and further research is ongoing in this area. However, orlistat is an FDA-approved medication for children aged 12 years and older with obesity. In rare genetic conditions such as proopiomelanocortin and leptin deficiency, melanocortin 4 receptor agonists like setmelanotide have received FDA approval for children aged six and older.
Continued research and evaluation of pharmacological treatments for pediatric obesity are necessary to expand the available options and ensure their safety and effectiveness in this population. The focus remains on a comprehensive approach that combines behavioral interventions, lifestyle modifications, and when appropriate, pharmacological interventions to address the complex nature of pediatric obesity.
medtigo
Childhood Obesity
Updated :
June 21, 2024
Childhood and adolescent obesity is a multifaceted and widespread health issue that often persists over time. It is characterized by a BMI equal to or greater than the 95th percentile for age and gender in children aged two years and older. In cases of severe obesity, the BMI threshold is equal to or greater than the 120th percentile.
For younger children, the Centers for Disease Control (CDC) recommend utilizing age, gender, and weight-for-length charts provided by the World Health Organization, instead of relying on BMI. In the United States, the prevalence of obesity in children has increased more than threefold since the 1960s, with rates tending to rise with age. Failing to prevent, identify, and address childhood obesity leads to concurrent health issues in children that often persist into adulthood.
Between 1963 -2000, there was a significant rise in the prevalence of obesity among children aged 6 to 11, increasing from 4.2% to 15.3%. The rate of obesity is even higher among adolescents, with 20.6% of 12 to 19-year-olds being affected. In the United States, approximately 13.5 million adolescents struggle with obesity.
There are notable disparities in obesity rates across different racial and ethnic groups, with non-Hispanic Black and Mexican American children exhibiting higher rates than non-Hispanic White children.
Factors contributing to these disparities include the educational level and income of parents, limited access to healthy food options, and a lack of safe opportunities for physical activity. Furthermore, children with disabilities such as autism and intellectual disabilities face an increased risk of developing obesity.
Neuroendocrine feedback mechanisms play a crucial role in regulating appetite and satiety. Various gastrointestinal hormones, such as ghrelin, stimulate appetite, while hormones like GLP-1, Peptide YY, CCK, and vagal neural feedback inhibit appetite and promote feelings of satiety. Adipose tissue also provides feedback on energy stores through hormones like adiponectin and leptin, which act as satiety signals.
These hormones relay feedback to the arcuate nucleus in the hypothalamus, which, in turn, sends behavioral and autonomic signals to the solitary tract nucleus in the brainstem, leading to the secretion of gastrointestinal hormones. Neuropeptides in the brain, including PYY, AgRP, and orexin, stimulate appetite, whereas melanocortin and alpha-melanocyte-stimulating hormones promote satiety. Genetic deficiencies in MCR4 have been associated with increased food-seeking behavior.
Insufficient sleep has been linked to decreased levels of circulating leptin, increased levels of ghrelin, and heightened self-reported hunger. The interaction between the gut, adipose tissue, and brain maintains a delicate balance between appetite stimulation and adiposity. Mutations in genes involved in the secretion of these hormones have attracted interest in terms of epigenetic modifications and their potential as therapeutic targets.
The development of obesity is influenced by a array of factors, making its etiology complex and multifaceted. Genetic, biological, environmental, socioeconomic, and cultural factors all contribute to the onset of obesity. While genetics and biology are predetermined, the other factors can be modified through interventions. These include the eating, sleeping, and exercise behaviors within a family, the availability of nutritious food options in schools and communities, access to safe environments for physical activity, and the impact of adverse childhood experiences.
When calorie intake exceeds energy expenditure, weight gain occurs, eventually leading to obesity. Although genetic factors play a role, they influence less than other factors. Changes in food preferences over the past few decades, driven by marketing strategies and the increased availability of high calorie processed foods such as fast food and sugary beverages, have contributed to the rise in obesity rates.
Consumption of these energy-dense foods, larger portion sizes, and increased snacking have been strongly associated with the significant increase in obesity in developed nations. Additionally, reduced levels of physical activity and increased sedentary behaviors, such as prolonged screen time from smartphones, computers, televisions, and video games, have contributed to the obesity problem. Cultural factors influence feeding patterns and food choices, and children often model their eating behaviors after their parents and families from a very young age.
Research shows that higher parental education and the establishment of structured family meals have a positive impact on children’s healthy food choices. Factors such as families eating together, exposing children to a variety of nutritious food options, and avoiding distractions like television during meals create a supportive food environment that reduces the risk of obesity development. Several additional risk factors have been identified that can predispose individuals to obesity.
Perinatal and postnatal conditions such as elevated maternal BMI during pregnancy, high birth weight, rapid weight gain during infancy and early childhood, and breastfeeding versus formula feeding can all impact obesity risk. Environmental chemicals, the composition of gut microbiota, early use of antibiotics, and adverse life experiences are also being explored as potential risk factors for obesity.
Timely identification and intervention in cases of obesity are essential for reducing associated health complications and improving long-term outcomes. As the burden of complications tends to escalate with age and severity, early diagnosis and treatment provide the most significant opportunity for maintaining good health.
When lifestyle modifications and behavioral interventions prove ineffective, healthcare professionals should promptly refer patients for pharmacological and surgical interventions. Failing to provide appropriate treatment can result in children with obesity transitioning into adulthood with obesity, putting them at risk for enduring negative health consequences.
Clinical History
The examiner should confront if the family has concerns regarding the child’s growth and weight and why. Prenatal factors such as gestational diabetes or maternal weight gain during pregnancy should be reviewed as they may increase the likelihood of obesity. Birth and perinatal history should be assessed, including information about intrauterine growth retardation followed by rapid catch-up growth or having a baby with a large size for gestational age.
Exploring meal composition, feeding patterns, snacking habits, and screen time can help identify potential causes of disproportionate weight gain. Assessing the type and duration of physical activity undertaken by the child. Analyzing the weight and height growth charts for any sudden changes in height, weight, and BMI trajectories may indicate underlying factors. Certain genetic conditions may present with excessive appetite and food-seeking conducts.
Genetic susceptibility might be considered if family members have undergone bariatric surgery for severe obesity or if obesity is observed across multiple generations. The presence of hypertension, diabetes, or cardiovascular disease in family members also increases the child’s risk of developing similar conditions. Parental obesity is a significant risk factor, likely influenced by genetics and social determinants of health. Clinicians should help families understand that childhood obesity increases the likelihood of developing several chronic diseases.
If there is a history of significant head trauma preceding sudden weight gain, a hypothalamic cause may be suspected. Symptoms such as easy bruising, muscle weakness, fatigue, and central obesity may indicate Cushing syndrome. Dry skin, cold intolerance, and anterior neck swelling may suggest hypothyroidism. However, it is important to note that less than 1% of children with obesity will be diagnosed with an endocrine cause, despite some families attributing weight gain to hormone imbalances. Additionally, a review of medications associated with obesity, such as steroids, antipsychotics (e.g., risperidone), and antiepileptics (e.g., valproate), can help identify drug-induced obesity.
Physical Examination
The physical examination should include calculating the BMI, and accurate BP measurement using an appropriately sized cuff is essential. A comprehensive head-to-toe examination should follow to identify potential causes and complications of obesity.
Facial and body dysmorphisms can provide clues to genetic disorders. Instances include hypogonadism, almond-shaped eyes, short neck, small hands and feet indicative of Prader-Willi syndrome, hypotonia, upward slanting eyes, and transverse palmar creases indicative of Down syndrome, as well as central obesity, round face, and more fatty tissue between the shoulders.
Cognitive impairment may suggest the presence of a genetic syndrome. Short stature may be associated with Albright hereditary osteodystrophy or hormone deficiencies. A specialist should further evaluate eye findings such as papilledema (indicating pseudotumor cerebri), nystagmus, and retinal degeneration (associated with Bardet-Biedl syndrome).
Skin changes such as acanthosis nigricans, acne, and hirsutism may indicate insulin resistance or polycystic ovary syndrome. Assessing sexual maturity can help identify premature adrenarche in obese girls. Dyspnea and wheezing may indicate asthma, hepatomegaly, and abdominal tenderness, suggesting non-alcoholic fatty liver disease. Knee and Hip mobility restrictions may be signs of slipped capital femoral epiphysis and Blount disease.
Differential Diagnoses
Hypothyroidism
Growth Hormone Deficiency
Cushing Syndrome
The management of pediatric obesity focuses on treating obesity itself and its associated comorbidities, aiming for weight loss, prevention of further weight gain, and improvement of complications. Behavioral change is fundamental in this approach. Family-based interventions play a crucial role in reducing BMI. T
hese interventions include limiting the consumption of sweetened beverages and fast food, increasing the intake of fruits and vegetables, and promoting increased physical activity. While there is no sufficient evidence to support the use of weight loss medications as a standalone therapy in pediatric patients, they are recommended as adjuncts when intensive behavioral interventions alone have not been successful.
It should be noted that many medications commonly used in adults have not received FDA approval for use in children, and further research is ongoing in this area. However, orlistat is an FDA-approved medication for children aged 12 years and older with obesity. In rare genetic conditions such as proopiomelanocortin and leptin deficiency, melanocortin 4 receptor agonists like setmelanotide have received FDA approval for children aged six and older.
Continued research and evaluation of pharmacological treatments for pediatric obesity are necessary to expand the available options and ensure their safety and effectiveness in this population. The focus remains on a comprehensive approach that combines behavioral interventions, lifestyle modifications, and when appropriate, pharmacological interventions to address the complex nature of pediatric obesity.
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