Childhood Obesity: Causes and Effects
Introduction, related effects, obesity control, essay voice-over.
Children obesity is an acute problem that is frequently met in the modern society. An unhealthy diet and the abundance of the junk food in the children’s menu leads to their gaining weight rapidly (Scherer, 2011). In order to address this problem properly, it is essential to examine its roots as well as to identify the ways of performing a positive change. A particular focus of the paper will be put on determining the ways school menus can be improved as the major part of children meals is consumed at school.
This disorder is brought about with varied combination of factors. First and foremost, it can be retrieved hereditary from the parents (Haerens, 2012). Family environment and genetics may influence a child’s condition largely in terms of obesity. Childhood obesity is a result of intertwine between environmental factors and genetics. The possession of two similar samples of alleles also recognized as FTO increases largely the risks of obesity.
There is a strong probability that parents’ obesity will be further transmitted to their children (Haerens, 2012). Other factors contributing to this condition is the lack of exercise, the child’s body type, psychological issues and unhealthy eating habits. The consumption of large quantities of junk food may likewise contribute to the development of obesity because most of the junk food always contains a large scope of calories and cholesterol (Scherer, 2011).
Most of the obese children from African and Hispanic communities lack exercise as their parents do not let them go outside in the fear of the dangers their children are always exposed to in the streets. It would be unfair to claim that these fears are ungrounded – these areas show high risks of being kidnapped by gangs as well as being abused sexually or hooked on drugs. Another factor that contributes to the increase in children’s obesity is the development of technologies (Haerens, 2012). Hence, the variety of the online games prevents children from going outside. In fact, they no more experience the need for live communication as their gadgets enable them to maintain virtual contacts. As a result, the physical activity of the modern children is evidently insufficient.
Family practices are another serious factor that leads to obesity in children (Haerens, 2012). Most mothers in these days do not exclusively breastfeed infants and introduce them to formulas very early. Parents are too concerned about their children’s safety. As a result, they prefer their children travelling by bus whatever short the destination (Scherer, 2011). The excessive care prevents children from the natural development, making them more exposed to the development of obesity (Haerens, 2012).
Another critical scope of factors is psychological triggers. Thus, psychological factors that lead to obesity include stress and anxiety (Koplan, Liverman & Kraak, 2007). Some people tend to overeat when being stressed or upset, and children are not an exception. When exposed to stress they tend to eat a lot to reduce stress hence their bodies absorb an excessive amount of energy which is further stored – as a result, a child is getting gradually obese (Scherer, 2011).
Obesity implies a series of associated effects. Some of the effects might reside in such health disorders as high blood pressure, strokes, heart diseases and even diabetes 2 (Haerens, 2012). These diseases reduce the children’s life span to five years. In most cases, children with obesity turn into obese adults in future. As long as children are always extra big physically, they tend to have low self-esteem and are commonly discriminated by other children (Haerens, 2012).
As a consequence, children get depressed because they see assume themselves to be different from other children and they are also teased by their classmates (Haerens, 2012). It is also empirically proved that children with obesity tend to age faster because of the distorted balance. In addition, they are more likely to have skin related diseases and get infected easily. Finally, it is the market policy that contributes to the growth of obese children. Hence, the availability of cheap foods in the market prompts families to compose unhealthy menus (Scherer, 2011).
Obesity can be controlled by changing unhealthy eating patterns into the healthy habits (Haerens, 2012). This can be done by eating balanced diet foods and reducing the number of the unhealthy products consumed. Exercise also help to reduce the excessive weight as they assist individuals in burning out the extra fats in their bodies (Haerens, 2012). Those children who are obese due to their genetics should also seek medical attention so that they can learn which type of obesity they have and what kind of lifestyle they should adopt.
Parents should be consulted on exclusive breastfeeding of their babies up to six months to eliminate any chances of children getting obese from the early childhood (Haerens, 2012). These formulas have a lot of chemicals and introducing babies to them does not only expose them to the risk of being obese but also implies other diseases.
At school, playgrounds should be made available for children to play. In addition, teachers should encourage children to perform some physical activity during the breaks. Most importantly, school caterers should focus on composing healthy menus rather than providing the largest quantities of food at the lowest price possible. It is assumed that the problem of childhood obesity should be treated complexly. Otherwise stated, both families and school staff should be involved in resolving it.
Haerens, M. (2012). Obesity . Detroit: Greenhaven Press.
Koplan, J., Liverman, C., & Kraak, V. (2007). Preventing childhood obesity . Washington, D.C.: National Academies Press.
Scherer, L. (2011). Obesity . Farmington Hills, MI: Greenhaven Press.
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- Patient Care & Health Information
- Diseases & Conditions
- Childhood obesity
Childhood obesity is a serious medical condition that affects children and adolescents. It's particularly troubling because the extra pounds often start children on the path to health problems that were once considered adult problems — diabetes, high blood pressure and high cholesterol. Childhood obesity can also lead to poor self-esteem and depression.
One of the best strategies to reduce childhood obesity is to improve the eating and exercise habits of your entire family. Treating and preventing childhood obesity helps protect your child's health now and in the future.
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- A Book: Mayo Clinic Guide to Raising a Healthy Child
Not all children carrying extra pounds are overweight. Some children have larger than average body frames. And children normally carry different amounts of body fat at the various stages of development. So you might not know by how your child looks if weight is a health concern.
The body mass index (BMI), which provides a guideline of weight in relation to height, is the accepted measure of overweight and obesity. Your child's doctor can use growth charts, the BMI and, if necessary, other tests to help you figure out if your child's weight could pose health problems.
When to see a doctor
If you're worried that your child is putting on too much weight, talk to his or her doctor. The doctor will consider your child's history of growth and development, your family's weight-for-height history, and where your child lands on the growth charts. This can help determine if your child's weight is in an unhealthy range.
Lifestyle issues — too little activity and too many calories from food and drinks — are the main contributors to childhood obesity. But genetic and hormonal factors might play a role as well.
Many factors — usually working in combination — increase your child's risk of becoming overweight:
- Diet. Regularly eating high-calorie foods, such as fast foods, baked goods and vending machine snacks, can cause your child to gain weight. Candy and desserts also can cause weight gain, and more and more evidence points to sugary drinks, including fruit juices and sports drinks, as culprits in obesity in some people.
- Lack of exercise. Children who don't exercise much are more likely to gain weight because they don't burn as many calories. Too much time spent in sedentary activities, such as watching television or playing video games, also contributes to the problem. TV shows also often feature ads for unhealthy foods.
- Family factors. If your child comes from a family of overweight people, he or she may be more likely to put on weight. This is especially true in an environment where high-calorie foods are always available and physical activity isn't encouraged.
- Psychological factors. Personal, parental and family stress can increase a child's risk of obesity. Some children overeat to cope with problems or to deal with emotions, such as stress, or to fight boredom. Their parents might have similar tendencies.
- Socioeconomic factors. People in some communities have limited resources and limited access to supermarkets. As a result, they might buy convenience foods that don't spoil quickly, such as frozen meals, crackers and cookies. Also, people who live in lower income neighborhoods might not have access to a safe place to exercise.
- Certain medications. Some prescription drugs can increase the risk of developing obesity. They include prednisone, lithium, amitriptyline, paroxetine (Paxil), gabapentin (Neurontin, Gralise, Horizant) and propranolol (Inderal, Hemangeol).
Childhood obesity often causes complications in a child's physical, social and emotional well-being.
Physical complications of childhood obesity may include:
- Type 2 diabetes. This chronic condition affects the way your child's body uses sugar (glucose). Obesity and a sedentary lifestyle increase the risk of type 2 diabetes.
- High cholesterol and high blood pressure. A poor diet can cause your child to develop one or both of these conditions. These factors can contribute to the buildup of plaques in the arteries, which can cause arteries to narrow and harden, possibly leading to a heart attack or stroke later in life.
- Joint pain. Extra weight causes extra stress on hips and knees. Childhood obesity can cause pain and sometimes injuries in the hips, knees and back.
- Breathing problems. Asthma is more common in children who are overweight. These children are also more likely to develop obstructive sleep apnea, a potentially serious disorder in which a child's breathing repeatedly stops and starts during sleep.
- Nonalcoholic fatty liver disease (NAFLD). This disorder, which usually causes no symptoms, causes fatty deposits to build up in the liver. NAFLD can lead to scarring and liver damage.
Social and emotional complications
Children who have obesity may experience teasing or bullying by their peers. This can result in a loss of self-esteem and an increased risk of depression and anxiety.
To help prevent excess weight gain in your child, you can:
- Set a good example. Make healthy eating and regular physical activity a family affair. Everyone will benefit and no one will feel singled out.
- Have healthy snacks available. Options include air-popped popcorn without butter, fruits with low-fat yogurt, baby carrots with hummus, or whole-grain cereal with low-fat milk.
- Offer new foods multiple times. Don't be discouraged if your child doesn't immediately like a new food. It usually takes multiple exposures to a food to gain acceptance.
- Choose nonfood rewards. Promising candy for good behavior is a bad idea.
- Be sure your child gets enough sleep. Some studies indicate that too little sleep may increase the risk of obesity. Sleep deprivation can cause hormonal imbalances that lead to increased appetite.
Also, be sure your child sees the doctor for well-child checkups at least once a year. During this visit, the doctor measures your child's height and weight and calculates his or her BMI . A significant increase in your child's BMI percentile rank over one year may be a possible sign that your child is at risk of becoming overweight.
- Helping your child who is overweight. National Institute of Diabetes and Digestive and Kidney Diseases. https://www.niddk.nih.gov/health-information/weight-management/helping-your-child-who-is-overweight. Oct. 14, 2020.
- Childhood obesity causes and consequences. Centers for Disease Control and Prevention. https://www.cdc.gov/obesity/childhood/causes.html. Accessed Oct. 14, 2020.
- Kliegman RM, et al. Overweight and obesity. In: Nelson Textbook of Pediatrics. 21st ed. Elsevier; 2020. https://www.clinicalkey.com. Accessed Oct. 14, 2020.
- Hay WW, et al., eds. Normal childhood nutrition and its disorders. In: Current Diagnosis & Treatment: Pediatrics. 25th ed. McGraw Hill; 2020. https://accessmedicine.mhmedical.com. Accessed Oct. 20, 2020.
- Skelton JA. Management of childhood obesity in the primary care setting. https://www.uptodate.com/contents/search. Accessed Oct. 14, 2020.
- Klish WJ, et al. Definition, epidemiology and etiology of obesity in children and adolescents. https://www.uptodate.com/contents/search. Accessed Oct. 14, 2020.
- Polfuss ML, et al. Childhood obesity: Evidence-based guidelines for clinical practice — Part one. Journal of Pediatric Health Care. 2020; doi:10.1016/j.pedhc.2019.12.003.
- Davis RL, et al. Childhood obesity: Evidence-based guidelines for clinical practice — Part two. Journal of Pediatric Health Care. 2020; doi:10.1016/j.pedhc.2020.07.011.
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Obesity effects on child health.
Palanikumar Balasundaram ; Sunil Krishna .
Last Update: April 10, 2023 .
- Continuing Education Activity
Obesity in childhood is the most challenging public health issue in the twenty-first century. Childhood obesity is associated with increased morbidity and premature death. Prevention of obesity in children is a high priority in the current situation. This activity reviews the etiology, pathophysiology, and consequence of childhood obesity and also highlights the role of the interprofessional team in the prevention and management of childhood obesity.
- Outline the definition of childhood obesity.
- Describe the etiology and pathophysiology of childhood obesity.
- Summarize the consequences of childhood obesity.
- Explain how interprofessional teamwork can improve effective management interventions for childhood obesity.
Obesity in childhood is the most challenging public health issue in the twenty-first century. It has emerged as a pandemic health problem worldwide. The children who are obese tend to stay obese in adulthood and prone to increased risk for diabetes and cardiac problems at a younger age. Childhood obesity is associated with increased morbidity and premature death.  Prevention of obesity in children is a high priority in the current situation.
The prevalence of childhood obesity has alarmingly increased. The overall burden of obesity has almost tripled since 1975. However, an eightfold increase in obesity burden in the 5 to 19 years age group has been noted between 1975 and 2016.  Though childhood obesity is more prevalent in developed countries, the prevalence is increasing even in developing countries.  Currently, about 18.5% of US children present with obesity. Among boys, obesity is more prevalent in the school-age group (6 to 11 years), whereas in girls, it is more prevalent in adolescents (12 to 19 years). The prevalence of childhood obesity among boys and girls was not significantly different overall or by age groups. 
The word obesity infers the deposition of excessive fat in the body. Different methods can directly measure body fat like skinfold thickness, hydro densitometry, bioelectrical impedance, and air displacement plethysmography.  These methods are not readily available in the clinical setting and are expensive. Body mass index (BMI) provides an economical method to assess body fat indirectly. BMI is measured using a formula [BMI = weight (kg)/ height (m)^2].   As growth in children varies with age and sex, so do the norms for BMI. The following definitions are used to classify weight status based on BMI for children from 2 to 20 years of age.  
- Overweight – 85th to less than the 95th percentile.
- Obese (class 1) – 95th percentile or greater
- Severe (class II) obesity – ≥ 120% of 95th percentile (99th percentile) or ≥ 35 kg/m^2 (whichever is lower)
- Class III obesity is a subcategory of severe obesity and is defined as BMI ≥140 % of 95th percentile or ≥ 40 kg/m^2.
The World Health Organization (WHO) recommends using BMI Z-score cut-offs of >1, > 2, and > 3 to define at risk of overweight, overweight, and obesity, respectively.  Z-score is measured in terms of standard deviations from the mean.
- Issues of Concern
Etiology and Pathophysiology
The complex interaction of individual and environmental factors plays a crucial role in developing obesity. The most important factors contributing to childhood obesity are summarized below.
Changes in the environment in the past few decades in terms of easy access/ affordability of high-calorie fast food, increased portion size, increased intake of sugary beverages, and sedentary lifestyles are associated with increased incidence of obesity.  Increasing use of electronic devices [television, tablets, smartphone, videogames] by children has led to limited physical activity, disruption of the sleep-wake cycle, depression of metabolic rate, and poor eating patterns. 
Feeding patterns in infancy have a long-term effect on developing obesity later on in life. It has been shown that breastfeeding in the first year of life is inversely associated with weight gain and obesity.  This association was much more significant if the child was exclusively breastfed compared to having added formula or solid food. Despite concerns about the risk for obesity in preterm and SGA infants receiving calorie and protein supplementation, it has been shown to improve catch-up growth without increasing the risk of obesity.  High protein intake in the initial two years of life has also been postulated to increase weight gain later in childhood.
There is a complex interaction between the neural, hormonal, and gut-brain axis affecting hunger and satiety. Hypothalamus regulates appetite and is influenced by key hormones, ghrelin, and leptin. Ghrelin is released from the stomach and stimulates hunger (orexigenic), whereas leptin is mainly secreted from adipose tissue and suppresses appetite (anorexigenic). Several other hormones like neuropeptide Y and agouti-related peptide stimulate hunger, while pro-melanocortin and α-melanocyte-stimulating hormone suppress hunger.  These hormones control energy balance by stimulating the hunger and satiety centers in the arcuate nucleus of the hypothalamus through various signaling pathways. Stress-related psychiatric disorders with associated abnormal sleep-wake cycles can also lead to increased ghrelin levels and, in turn, increase appetite.
The gut microbiome includes the trillions of microorganisms that inhabit the human gut. Alterations in the gut microbiome can lead to weight gain through numerous pathways.  The dominant gut florae are Firmicutes and Bacteroidetes (90%), Proteobacteria , Actinobacteria , and Fusobacteria . These bacteria have a symbiotic relationship with their host. They can be affected by various factors, such as gestational age at birth, premature rupture of membranes, mode of delivery of the infant, type of feeding, feeding practices, and antibiotics usage. The maturation of gut flora occurs from birth to adulthood and is determined by various genetic factors, diet, lifestyle, and environment. Gut microbiota helps maintain the mucosal barrier, nutrient digestion (especially the synthesis of short-chain fatty acids), and immune response against pathogens. The imbalance of the gut microbiome (dysbiosis), leading to increased production of short-chain fatty acids, has been linked to developing obesity and other medical conditions, such as type 2 Diabetes Mellitus, Metabolic syndrome, anxiety, and depression. 
Obesity can be either monogenic, syndromic, or polygenic types. Monogenic obesity is uncommon, occurring in 3% to 5% of obese children.  Mutations in genes for leptin, leptin receptor, proopiomelanocortin, and melanocortin-4 receptor can lead to obesity. Monogenic type presents in early childhood with unusual feeding behaviors and severe obesity.
Genetic syndromes causing severe obesity include
- Prader Willi syndrome: Early growth faltering followed by hyperphagia and increased weight gain by 2 to 3 years. The mild or moderate cognitive deficit, microcephaly, short stature, hypotonia, almond-shaped eyes, high-arched palate, narrow hands/feet, delayed puberty are common features.
- Alstrom syndrome: Blindness, deafness, acanthosis nigricans, chronic nephropathy, type 2 diabetes, cirrhosis, primary hypogonadism in males, and normal cognition are common features in Alstrom syndrome.
- Bardet Biedl syndrome: Intellectual disability, hypotonia, retinitis pigmentosa, polydactyly, hypogonadism, glucose intolerance, deafness, and renal disease are the features in Bardet Biedl syndrome.
- Other syndromes include Beckwith-Weideman syndrome and Cohen syndrome.
Polygenic obesity is much more common and is caused by a complex interaction between multiple genetic variants and the environment known as gene-environment interaction (GEI). When a child with genotype variants conferring risk for obesity interacts with various environmental factors predisposing to obesity, there is a tendency for decreased physical activity, increased food intake, and body fat storage. Early life environment starting with maternal nutrition during the prenatal or early postnatal period and early childhood adverse environmental or psychosocial stressors can lead to epigenetic changes leading to obesity.
Endocrine causes constitute less than 1% of cases of obesity in children.  It is usually associated with mild to moderate obesity, short stature, or hypogonadism. These include cortisol excess [steroid medications or Cushing syndrome], hypothyroidism, growth hormone deficiency, and pseudohypoparathyroidism.
Numerous medications can cause weight gain. These include antiepileptics, antidepressants, antipsychotics, diabetes medications [insulin, sulfonylureas, thiazolidinediones], glucocorticoids, progestins, antihistamines [cyproheptadine], alpha-blockers [terazosin], and beta-blockers [propranolol]. Close monitoring for excessive weight gain should be done when any of these medications are used in children.
Endocrine-disrupting chemicals, such as bisphenol A and dichlorodiphenyltrichloroethane, have been hypothesized to predispose to obesity by modulating estrogen receptors and possibly metabolic programming. 
Few studies in animal models have proven that obesity can be triggered by infection with adenovirus. However, human studies have found conflicting results.
- Clinical Significance
Childhood obesity significantly impacts both physical and psychological health. Obesity can lead to severe health conditions, including non-insulin-dependent diabetes, cardiovascular problems, bronchial asthma, obstructive sleep apnea (OSA), hypertension, hepatic steatosis, gastroesophageal reflux (GER), and psychosocial issues. The preventive and therapeutic interventions in childhood obesity are crucial in decreasing the burden of comorbid health conditions.
Metabolic syndrome, also named syndrome X, is a cluster of risk factors specific for cardiovascular diseases such as hypertension, glucose intolerance, dyslipidemia, and abdominal obesity that commonly occur in obese children or adolescents. Insulin resistance, hyperinsulinemia, and oxidative stress are the underlying factors contributing to metabolic syndrome. 
Atherogenic dyslipidemia is common in obese children and adolescents. A fasting lipoprotein level needs to be obtained in all children with obesity. Elevated triglycerides (TG) and Free fatty acid (FFA) levels, decreased HDL (high-density lipoprotein) cholesterol levels, and normal or mildly increased serum LDL (low-density lipoprotein) cholesterol levels are common findings in childhood obesity.  Hyperinsulinemia and insulin resistance in childhood obesity promotes hepatic delivery of FFA for triglyceride synthesis and sequestration into TG-rich lipoproteins. 
Childhood obesity quadruples the risk of developing glucose intolerance and non-insulin-dependent diabetes mellitus (NIDDM or Type 2 diabetes). Over 85% of children with NIDDM are either overweight or obese at diagnosis.  Acanthosis nigricans is an increased pigmentation and thickness of the skin in intertriginous folds, and it is usually associated with glucose intolerance in children and adolescents. Fasting insulin and glucose should be included in the evaluation of childhood obesity. The risk factors for type 2 non-insulin-dependent diabetes and metabolic syndrome include,
- children with BMI 85th to 95th percentile along with,
- immediate family history of type 2 diabetes
- signs of insulin resistance such as acanthosis nigricans, dyslipidemia, hypertension, and polycystic ovarian syndrome.
- Children with BMI >95th percentile regardless of family history or associated features. 
The most significant risk factor for pediatric hypertension is the high body mass index. One-fourth of obese children can have hypertension. Adipocyte is not only a storage depot for fat but is also an active endocrinological cell. The pro-inflammatory adipokines (leptin, resistin, and IL-6) lead to an increase in sympathetic nervous system (SNS) activation, which preferentially impacts the renal vascular beds.  Hypertension risk in childhood obesity can also be explained due to hyperinsulinemia. Hyperinsulinemia causes hypertension through secondary mechanisms such as increased renal sodium retention, increased intracellular free calcium, and increased SNS activity.  Dietary therapy, along with exercise, effectively decreases blood pressure.
Pediatric liver disease is a severe complication of childhood obesity. Obesity-related non-alcoholic fatty liver disease (NAFLD) spectrum includes fatty liver, steatohepatitis, cirrhosis, and hepatocellular carcinoma.  Hyperinsulinemia in childhood obesity plays a significant role in contributing to hepatic steatosis. Gradual weight loss with regular exercise and diet with less refined carbohydrates and low-fat help normalize hepatic enzymes and resolve hepatic steatosis. 
The prevalence of cholelithiasis is high among adolescents with obesity, and the association is more robust in girls than in boys. Increased cholesterol synthesis and cholesterol saturation of bile contribute to cholelithiasis among adolescents with obesity.   Cholelithiasis occurs even more frequently with weight reduction. Almost half of the cases of cholecystitis in adolescents may be associated with obesity.
Overweight or obese children have been observed to have a higher prevalence of asthma and asthma exacerbations. The link between asthma and obesity is mediated through abnormal inflammatory and oxidant stress, chest restriction with airway narrowing, and obesity-related comorbidities such as obstructive sleep apnea and gastroesophageal reflux. 
Idiopathic Intracranial Hypertension
Idiopathic intracranial hypertension (IIH) is an uncommon disease of childhood and adolescence characterized by increased intracranial pressure without any identifiable cause. Almost half of the children who present with this syndrome may be obese and also have more IIH symptoms at onset.  The disease is characterized by elevated intracranial pressure. IIH presents with headaches and may lead to severe visual impairment or blindness. The potential for visual impairment indicates the need for aggressive treatment of obesity in patients with IIH.
Obesity and overweight are crucial risk factors for obstructive sleep apnea (OSA). Neurocognitive deficits and excessive daytime sleepiness are common among obese children with sleep apnea.  Obesity hypoventilation syndrome may represent a long-term consequence of sleep apnea and is associated with a high mortality rate. Aggressive therapy is warranted for obese children with this syndrome. Obesity management such as increased physical activity and a healthy diet are recommended for OSA treatment, as well as surgical procedures, if appropriate.
Fractures, musculoskeletal discomfort, and lower extremity malalignment such as Blount disease and slipped capital femoral epiphyses are more common in overweight than non-overweight children and adolescents.  Blount disease is a disorder of the proximal tibial growth plate, which results in progressive bowing of the tibia. Although the prevalence of Blount disease is low, approximately two-thirds of Blount disease patients may be obese. Slipped capital femoral epiphysis occurs due to epiphyseal plate disruption. Between 30% and 50% of patients with slipped capital femoral epiphysis are overweight.
Polycystic Ovary Disease
Obesity is frequently associated with polycystic ovary disease (PCOD). Up to 30% of women with PCOD may be obese. Hyperandrogenism and hyperinsulinemia often accompany PCOD. Obesity increases the risk of PCOD through insulin resistance and compensatory hyperinsulinemia, which increases androgen production and decreases sex hormone-binding globulin, thereby increasing the bioavailability of androgen. Adolescents with PCOD are at increased risk for metabolic syndrome and glucose intolerance. Weight loss represents an important therapeutic target in obese adolescents with PCOD.
Persistence of obesity into adulthood
About 15% to 30% of adults with obesity were also obese in their childhood or adolescence.  The cardiovascular risk factors present in obese children or adolescents usually persist into adulthood. The change in body fat in obese adolescents can be a reasonable mediator contributing to the excess morbidity and mortality in later adulthood.
Children with obesity or overweight are more likely to experience low self-esteem and depression during adolescence. Negative psychological experiences trigger emotional eating, leading to an ongoing obesity-depression cycle. Children who are overweight or obese face bullying at school and are excluded from competitive physical activities. Overall, children with obesity have less social interaction and spend more time in sedentary activities. Numerous studies have confirmed the association of childhood obesity with ADHD and anxiety disorders. 
Children with overweight or obesity have a high prevalence of disordered eating behaviors, increasing the risk of developing eating disorders. The majority of adolescents with restrictive eating disorders report a history of obesity in the past. Binge eating increases the risk of obesity and type 2 diabetes.  Appropriate evaluation for eating disorders should be performed during the treatment planning of childhood obesity.
Children who are obese and have comorbid health problems like diabetes, asthma, or sleep apnea miss school more frequently, thereby affecting their school performance negatively.
- Enhancing Healthcare Team Outcomes
Prevention is the best intervention to decrease the prevalence of obesity. The pediatrician should explore the risk of obesity and overweight during every clinical visit for all children.
- Both bottle-fed and breastfed infants are at risk of overfeeding. However, overfeeding is more prevalent among bottle-fed infants. Exclusive breastfeeding and delayed initiation of solid foods may reduce the future risk of overweight.
- Skim milk is a safe replacement for whole milk after two years of age. Parents or caretakers should never use food like sweets for a reward. The entire family should have a balanced diet that comprises less than 30 percent of calories from fat. AAP recommends consuming a variety of vegetables and fruits, whole grains, proteins, low-fat dairies and decreasing the intake of sodium, saturated fats, and refined sugars beginning at the age of two years. 
- An essential step in preventing obesity is reducing sedentary time. Limit the screen time, including television, video games, or mobile, not more than 2 hours per day for more than six-year-old children and not more than 1 hour per day for 2-6 years of age group. AAP strongly recommends not allowing kids less than two years to have screen time. 
- Encourage physical activity for children. Children aged 3 to 5 years should be active throughout the day. Children and adolescents ages 6 to 17 years should be physically active for at least 60 minutes every day. 
- As per CDC, 60% of middle school kids and 70% of high school kids do not meet the standard sleep recommendations. AAP recommends that children aged 1 to 2 years sleep 11 to 14 hours per day, children 3 to 5 years sleep 10 to 13 hours, children 6 to 12 years sleep 9 to 12 hours, and adolescents aged 13 to 18 years should regularly sleep 8 to 10 hours.  Avoiding heavy meals close to bedtime, being physically active throughout the day, and removing electronic devices in the bedroom will help to get better sleep.
The pediatrician should explore for associated morbidity in all obese children. The detailed assessment in obese children should include assessing cardiac comorbidities, orthopedic complications, and psycho-social complications.
- Reasonable weight-loss goals should be initially 5 to 10 pounds (2 kg to 4.5 kg) or a rate of 1 to 4 pounds (0.5 to 2 kg) per month.
- Dietary management: Dieticians provide dietary prescriptions mentioning the total calories per day and recommended percentage of calories from carbohydrates, protein, and fat. The Traffic Light Plan is one method of providing dietary management. The Traffic Light Plan classifies foods as green (low energy density), yellow (moderate energy density), and red (high energy density). These categories help children in adopting healthier eating patterns. The dietician plays a significant role in guiding the diet plan for the patients.
- Physical activity: As per the fitness level, begin the physical activity with the goal of 30 minutes/day in addition to any school activity. Treatment should target gradually increasing the activity to 60 minutes per day. An exercise physiologist, along with the physician, can help the patients to achieve their target physical activity.
- Behavior modification: Primary care-based behavioral interventions such as self-monitoring, nutritional education, improvement of eating habits, increasing physical activity, attitude change, and rewards help manage childhood obesity.
- Family involvement: Review overall family activity and television viewing patterns and always involve parents in nutrition counseling. Family-based behavioral treatment is the most robust intervention for childhood obesity. 
- Psychotherapy: Behavioral therapy and Cognitive therapy are commonly used by the psychologist in the management of obesity. Behavioral therapy trains patients to act differently around food, and cognitive therapy trains patients how to change their thoughts and emotions related to food.
- None of the anorexiant medications are FDA approved for use in childhood obesity. Orlistat is the only FDA-approved medication for use in adolescents.
- Surgical procedures like gastric bypass have not been studied sufficiently in children to advise their use.
An interprofessional team that provides a holistic and integrated approach can help achieve the best possible outcomes. Collaboration, shared decision making, and communication are key elements for a good outcome. Multidisciplinary teams include a primary physician, a dietician, a nurse or nurse practitioner, a clinical exercise physiologist, and a psychologist. The interprofessional team can provide a comprehensive weight loss program that benefits the patients.
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Disclosure: Palanikumar Balasundaram declares no relevant financial relationships with ineligible companies.
Disclosure: Sunil Krishna declares no relevant financial relationships with ineligible companies.
This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.
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Review article, childhood and adolescent obesity: a review.
- 1 Division of Endocrinology, Diabetes and Metabolism, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, United States
- 2 Division of Adolescent Medicine, Department of Pediatrics, Medical College of Wisconsin Affiliated Hospitals, Milwaukee, WI, United States
- 3 Division of Adolescent Medicine, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, United States
Obesity is a complex condition that interweaves biological, developmental, environmental, behavioral, and genetic factors; it is a significant public health problem. The most common cause of obesity throughout childhood and adolescence is an inequity in energy balance; that is, excess caloric intake without appropriate caloric expenditure. Adiposity rebound (AR) in early childhood is a risk factor for obesity in adolescence and adulthood. The increasing prevalence of childhood and adolescent obesity is associated with a rise in comorbidities previously identified in the adult population, such as Type 2 Diabetes Mellitus, Hypertension, Non-alcoholic Fatty Liver disease (NAFLD), Obstructive Sleep Apnea (OSA), and Dyslipidemia. Due to the lack of a single treatment option to address obesity, clinicians have generally relied on counseling dietary changes and exercise. Due to psychosocial issues that may accompany adolescence regarding body habitus, this approach can have negative results. Teens can develop unhealthy eating habits that result in Bulimia Nervosa (BN), Binge- Eating Disorder (BED), or Night eating syndrome (NES). Others can develop Anorexia Nervosa (AN) as they attempt to restrict their diet and overshoot their goal of “being healthy.” To date, lifestyle interventions have shown only modest effects on weight loss. Emerging findings from basic science as well as interventional drug trials utilizing GLP-1 agonists have demonstrated success in effective weight loss in obese adults, adolescents, and pediatric patients. However, there is limited data on the efficacy and safety of other weight-loss medications in children and adolescents. Nearly 6% of adolescents in the United States are severely obese and bariatric surgery as a treatment consideration will be discussed. In summary, this paper will overview the pathophysiology, clinical, and psychological implications, and treatment options available for obese pediatric and adolescent patients.
Obesity is a complex issue that affects children across all age groups ( 1 – 3 ). One-third of children and adolescents in the United States are classified as either overweight or obese. There is no single element causing this epidemic, but obesity is due to complex interactions between biological, developmental, behavioral, genetic, and environmental factors ( 4 ). The role of epigenetics and the gut microbiome, as well as intrauterine and intergenerational effects, have recently emerged as contributing factors to the obesity epidemic ( 5 , 6 ). Other factors including small for gestational age (SGA) status at birth, formula rather than breast feeding in infancy, and early introduction of protein in infant's dietary intake have been reportedly associated with weight gain that can persist later in life ( 6 – 8 ). The rising prevalence of childhood obesity poses a significant public health challenge by increasing the burden of chronic non-communicable diseases ( 1 , 9 ).
Obesity increases the risk of developing early puberty in children ( 10 ), menstrual irregularities in adolescent girls ( 1 , 11 ), sleep disorders such as obstructive sleep apnea (OSA) ( 1 , 12 ), cardiovascular risk factors that include Prediabetes, Type 2 Diabetes, High Cholesterol levels, Hypertension, NAFLD, and Metabolic syndrome ( 1 , 2 ). Additionally, obese children and adolescents can suffer from psychological issues such as depression, anxiety, poor self-esteem, body image and peer relationships, and eating disorders ( 13 , 14 ).
So far, interventions for overweight/obesity prevention have mainly focused on behavioral changes in an individual such as increasing daily physical exercise or improving quality of diet with restricting excess calorie intake ( 1 , 15 , 16 ). However, these efforts have had limited results. In addition to behavioral and dietary recommendations, changes in the community-based environment such as promotion of healthy food choices by taxing unhealthy foods ( 17 ), improving lunch food quality and increasing daily physical activity at school and childcare centers, are extra measures that are needed ( 16 ). These interventions may include a ban on unhealthy food advertisements aimed at children as well as access to playgrounds and green spaces where families can feel their children can safely recreate. Also, this will limit screen time for adolescents as well as younger children.
However, even with the above changes, pharmacotherapy and/or bariatric surgery will likely remain a necessary option for those youth with morbid obesity ( 1 ). This review summarizes our current understanding of the factors associated with obesity, the physiological and psychological effects of obesity on children and adolescents, and intervention strategies that may prevent future concomitant issues.
Definition of Childhood Obesity
Body mass index (BMI) is an inexpensive method to assess body fat and is derived from a formula derived from height and weight in children over 2 years of age ( 1 , 18 , 19 ). Although more sophisticated methods exist that can determine body fat directly, they are costly and not readily available. These methods include measuring skinfold thickness with a caliper, Bioelectrical impedance, Hydro densitometry, Dual-energy X-ray Absorptiometry (DEXA), and Air Displacement Plethysmography ( 2 ).
BMI provides a reasonable estimate of body fat indirectly in the healthy pediatric population and studies have shown that BMI correlates with body fat and future health risks ( 18 ). Unlike in adults, Z-scores or percentiles are used to represent BMI in children and vary with the age and sex of the child. BMI Z-score cut off points of >1.0, >2.0, and >3.0 are recommended by the World Health Organization (WHO) to define at risk of overweight, overweight and obesity, respectively ( 19 ). However, in terms of percentiles, overweight is applied when BMI is >85th percentile <95th percentile, whereas obesity is BMI > 95th percentile ( 20 – 22 ). Although BMI Z-scores can be converted to BMI percentiles, the percentiles need to be rounded and can misclassify some normal-weight children in the under or overweight category ( 19 ). Therefore, to prevent these inaccuracies and for easier understanding, it is recommended that the BMI Z-scores in children should be used in research whereas BMI percentiles are best used in the clinical settings ( 20 ).
As BMI does not directly measure body fat, it is an excellent screening method, but should not be used solely for diagnostic purposes ( 23 ). Using 85th percentile as a cut off point for healthy weight may miss an opportunity to obtain crucial information on diet, physical activity, and family history. Once this information is obtained, it may allow the provider an opportunity to offer appropriate anticipatory guidance to the families.
Pathophysiology of Obesity
The pathophysiology of obesity is complex that results from a combination of individual and societal factors. At the individual level, biological, and physiological factors in the presence of ones' own genetic risk influence eating behaviors and tendency to gain weight ( 1 ). Societal factors include influence of the family, community and socio-economic resources that further shape these behaviors ( Figure 1 ) ( 3 , 24 ).
Figure 1 . Multidimensional factors contributing to child and adolescent obesity.
There is a complex architecture of neural and hormonal regulatory control, the Gut-Brain axis, which plays a significant role in hunger and satiety ( Figure 2 ). Sensory stimulation (smell, sight, and taste), gastrointestinal signals (peptides, neural signals), and circulating hormones further contribute to food intake ( 25 – 27 ).
Figure 2 . Pictorial representation of the Hunger-Satiety pathway a and the various hormones b involved in the pathway. a, Y1/Y5R and MC3/4 are second order neuro receptors which are responsible in either the hunger or satiety pathway. Neurons in the ARC include: NPY, Neuropeptide Y; AgRP, Agouti-Related Peptide; POMC, Pro-Opiomelanocortin; CART, Cocaine-and Amphetamine-regulated Transcript; α-MSH, α-Melanocyte Stimulating Hormone. b, PYY, Peptide YY; PP, Pancreatic Polypeptide; GLP-1, Glucagon-Like Peptide- I; OMX, Oxyntomodulin.
The hypothalamus is the crucial region in the brain that regulates appetite and is controlled by key hormones. Ghrelin, a hunger-stimulating (orexigenic) hormone, is mainly released from the stomach. On the other hand, leptin is primarily secreted from adipose tissue and serves as a signal for the brain regarding the body's energy stores and functions as an appetite -suppressing (anorexigenic) hormone. Several other appetite-suppressing (anorexigenic) hormones are released from the pancreas and gut in response to food intake and reach the hypothalamus through the brain-blood barrier (BBB) ( 28 – 32 ). These anorexigenic and orexigenic hormones regulate energy balance by stimulating hunger and satiety by expression of various signaling pathways in the arcuate nucleus (ARC) of the hypothalamus ( Figure 2 ) ( 28 , 33 ). Dysregulation of appetite due to blunted suppression or loss of caloric sensing signals can result in obesity and its morbidities ( 34 ).
Emotional dysfunction due to psychiatric disorders can cause stress and an abnormal sleep-wake cycles. These modifications in biological rhythms can result in increased appetite, mainly due to ghrelin, and can contribute to emotional eating ( 35 ).
Recently, the role of changes in the gut microbiome with increased weight gain through several pathways has been described in literature ( 36 , 37 ). The human gut serves as a host to trillions of microorganisms, referred to as gut microbiota. The dominant gut microbial phyla are Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria, Fusobacteria, and Verrucomicrobia, with Firmicutes and Bacteroidetes representing 90% of human gut microbiota ( 5 , 38 ). The microbes in the gut have a symbiotic relationship within their human host and provide a nutrient-rich environment. Gut microbiota can be affected by various factors that include gestational age at birth, mode of infant delivery, type of neonatal and infant feeding, introduction of solid food, feeding practices and external factors like antibiotic use ( 5 , 38 ). Also, the maturation of the bacterial phyla that occurs from birth to adulthood ( 39 ), is influenced by genetics, environment, diet, lifestyle, and gut physiology and stabilizes in adulthood ( 5 , 39 , 40 ). Gut microbiota is unique to each individual and plays a specific role in maintaining structural integrity, and the mucosal barrier of the gut, nutrient metabolism, immune response, and protection against pathogens ( 5 , 37 , 38 ). In addition, the microbiota ferments the indigestible food and synthesizes other essential micronutrients as well as short chain fatty acids (SCFAs') ( 40 , 41 ). Dysbiosis or imbalance of the gut microbiota, in particularly the role of SCFA has been linked with the patho-physiology of obesity ( 36 , 38 , 41 , 42 ). SCFAs' are produced by anaerobic fermentation of dietary fiber and indigestible starch and play a role in mammalian energy metabolism by influencing gut-brain communication axis. Emerging evidence has shown that increased ratio of Firmicutes to Bacteroidetes causes increased energy extraction of calories from diets and is evidenced by increased production of short chain fatty acids (SCFAs') ( 43 – 45 ). However, this relationship is not affirmed yet, as a negative relationship between SCFA levels and obesity has also been reported ( 46 ). Due to the conflicting data, additional randomized control trials are needed to clarify the role of SCFA's in obese and non-obese individuals.
The gut microbiota also has a bidirectional interaction with the liver, and various additional factors such as diet, genetics, and the environment play a key role in this relationship. The Gut- Liver Axis is interconnected at various levels that include the mucus barrier, epithelial barrier, and gut microbiome and are essential to maintain normal homeostasis ( 47 ). Increased intestinal mucosal permeability can disrupt the gut-liver axis, which releases various inflammatory markers, activates an innate immune response in the liver, and results in a spectrum of liver diseases that include hepatic steatosis, non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC) ( 48 , 49 ).
Other medical conditions, including type 2 Diabetes Mellitus, Metabolic Syndrome, eating disorders as well as psychological conditions such as anxiety and depression are associated with the gut microbiome ( 50 – 53 ).
Genetic causes of obesity can either be monogenic or polygenic types. Monogenic obesity is rare, mainly due to mutations in genes within the leptin/melanocortin pathway in the hypothalamus that is essential for the regulation of food intake/satiety, body weight, and energy metabolism ( 54 ). Leptin regulates eating behaviors, the onset of puberty, and T-cell immunity ( 55 ). About 3% of obese children have mutations in the leptin ( LEP ) gene and the leptin receptor (LEPR) and can also present with delayed puberty and immune dysfunction ( 55 , 56 ). Obesity caused by other genetic mutations in the leptin-melanocortin pathway include proopiomelanocortin (POMC) and melanocortin receptor 4 (MC4R), brain-derived neurotrophic factor (BDNF), and the tyrosine kinase receptor B (NTRK2) genes ( 57 , 58 ). Patients with monogenic forms generally present during early childhood (by 2 years old) with severe obesity and abnormal feeding behaviors ( 59 ). Other genetic causes of severe obesity are Prader Willi Syndrome (PWS), Alström syndrome, Bardet Biedl syndrome. Patients with these syndromes present with additional characteristics, including cognitive impairment, dysmorphic features, and organ-specific developmental abnormalities ( 60 ). Individuals who present with obesity, developmental delay, dysmorphic features, and organ dysfunction should receive a genetics referral for further evaluation.
Polygenic obesity is the more common form of obesity, caused by the combined effect of multiple genetic variants. It is the result of the interplay between genetic susceptibility and the environment, also known as the Gene-Environment Interaction (GEI) ( 61 – 64 ). Genome-wide association studies (GWAS) have identified gene variants [single nucleotide polymorphism (SNPs)] for body mass index (BMI) that likely act synergistically to affect body weight ( 65 ). Studies have identified genetic variants in several genes that may contribute to excessive weight gain by increasing hunger and food intake ( 66 – 68 ). When the genotype of an individual confers risk for obesity, exposure to an obesogenic environment may promote a state of energy imbalance due to behaviors that contribute to conserving rather than expending energy ( 69 , 70 ). Research studies have shown that obese individuals have a genetic variation that can influence their actions, such as increased food intake, lack of physical activity, a decreased metabolism, as well as an increased tendency to store body fat ( 63 , 66 , 67 , 69 , 70 ).
Recently the role of epigenetic factors in the development of obesity has emerged ( 71 ). The epigenetic phenomenon may alter gene expression without changing the underlying DNA sequence. In effect, epigenetic changes may result in the addition of chemical tags known as methyl groups, to the individual's chromosomes. This alteration can result in a phenomenon where critical genes are primed to on and off regulate. Complex physiological and psychological adjustment occur during infancy and can thereafter set the stage for health vs. disease. Developmental origins of health and disease (DOHaD) shows that early life environment can impact the risk of chronic diseases later in life due to fetal programming secondary to epigenetic changes ( 72 ). Maternal nutrition during the prenatal or early postnatal period may trigger these epigenetic changes and increase the risk for chronic conditions such as obesity, metabolic and cardiovascular disease due to epigenetic modifications that may persist and cause intergenerational effect on the health children and adults ( 58 , 73 , 74 ). Similarly, adverse childhood experiences (ACE) have been linked to a broad range of negative outcomes through epigenetic mechanisms ( 75 ) and promote unhealthy eating behaviors ( 76 , 77 ). Other factors such as diet, physical activity, environmental and psychosocial stressors can cause epigenetic changes and place an individual at risk for weight gain ( 78 ).
Eating behaviors evolve over the first few years of life. Young children learn to eat through their direct experience with food and observing others eating around them ( 79 ). During infancy, feeding defines the relationship of security and trust between a child and the parent. Early childhood eating behaviors shift to more self-directed control due to rapid physical, cognitive, communicative, and social development ( 80 ). Parents or caregivers determine the type of food that is made available to the infant and young child. However, due to economic limitations and parents having decreased time to prepare nutritious meals, consumption of processed and cheaper energy-dense foods have occurred in Western countries. Additionally, feeding practices often include providing large or super-sized portions of palatable foods and encouraging children to finish the complete meal (clean their plate even if they do not choose to), as seen across many cultures ( 81 , 82 ). Also, a segment of parents are overly concerned with dietary intake and may pressurize their child to eat what they perceive as a healthy diet, which can lead to unintended consequences ( 83 ). Parents' excessive restriction of food choices may result in poor self-regulation of energy intake by their child or adolescent. This action may inadvertently promote overconsumption of highly palatable restricted foods when available to the child or adolescent outside of parental control with resultant excessive weight gain ( 84 , 85 ).
During middle childhood, children start achieving greater independence, experience broader social networks, and expand their ability to develop more control over their food choices. Changes that occur in the setting of a new environment such as daycare or school allow exposure to different food options, limited physical activity, and often increased sedentary behaviors associated with school schedules ( 24 ). As the transition to adolescence occurs, physical and psychosocial development significantly affect food choices and eating patterns ( 25 ). During the teenage years, more independence and interaction with peers can impact the selection of fast foods that are calorically dense. Moreover, during the adolescent years, more sedentary behaviors such as video and computer use can limit physical exercise. Adolescence is also a period in development with an enhanced focus on appearance, body weight, and other psychological concerns ( 86 , 87 ).
Environmental changes within the past few decades, particularly easy access to high-calorie fast foods, increased consumption of sugary beverages, and sedentary lifestyles, are linked with rising obesity ( 88 ). The easy availability of high caloric fast foods, and super-sized portions, are increasingly common choices as individuals prefer these highly palatable and often less expensive foods over fruits and vegetables ( 89 ). The quality of lunches and snacks served in schools and childcare centers has been an area of debate and concern. Children and adolescents consume one-third to one-half of meals in the above settings. Despite policies in place at schools, encouraging foods, beverages, and snacks that are deemed healthier options, the effectiveness of these policies in improving children's dietary habits or change in obesity rate has not yet been seen ( 90 ). This is likely due to the fact that such policies primarily focus on improving dietary quality but not quantity which can impact the overweight or obese youth ( 91 ). Policies to implement taxes on sugary beverages are in effect in a few states in the US ( 92 ) as sugar and sugary beverages are associated with increased weight gain ( 2 , 3 ). This has resulted in reduction in sales of sugary drinks in these states, but the sales of these types of drinks has risen in neighboring states that did not implement the tax ( 93 ). Due to advancements in technology, children are spending increased time on electronic devices, limiting exercise options. Technology advancement is also disrupting the sleep-wake cycle, causing poor sleeping habits, and altered eating patterns ( 94 ). A study published on Canadian children showed that the access to and night-time use of electronic devices causes decreased sleep duration, resulting in excess body weight, inferior diet quality, and lower physical activity levels ( 95 ).
Infant nutrition has gained significant popularity in relation to causing overweight/obesity and other diseases later in life. Breast feeding is frequently discussed as providing protection against developing overweight/obesity in children ( 8 ). Considerable heterogeneity has been observed in studies and conducting randomized clinical trials between breast feeding vs. formula feeding is not feasible ( 8 ). Children fed with a low protein formula like breast milk are shown to have normal weight gain in early childhood as compared to those that are fed formulas with a high protein load ( 96 ). A recent Canadian childbirth cohort study showed that breast feeding within first year of life was inversely associated with weight gain and increased BMI ( 97 ). The effect was stronger if the child was exclusively breast fed directly vs. expressed breast milk or addition of formula or solid food ( 97 ). Also, due to the concern of poor growth in preterm or SGA infants, additional calories are often given for nutritional support in the form of macronutrient supplements. Most of these infants demonstrate “catch up growth.” In fact, there have been reports that in some children the extra nutritional support can increase the risk for overweight/obesity later in life. The association, however, is inconsistent. Recently a systemic review done on randomized controlled trials comparing the studies done in preterm and SGA infants with feeds with and without macronutrient supplements showed that macronutrient supplements may increase weight and length in toddlers but did not show a significant increase in the BMI during childhood ( 98 ). Increased growth velocity due to early introduction of formula milk and protein in infants' diet, may influence the obesity pathways, and can impact fetal programming for metabolic disease later in life ( 99 ).
General pediatricians caring for children with overweight/obesity, generally recommend endocrine testing as parents often believe that there may be an underlying cause for this condition and urge their primary providers to check for conditions such as thyroid abnormalities. Endocrine etiologies for obesity are rarely identified and patients with underlying endocrine disorders causing excessive weight gain usually are accompanied by attenuated growth patterns, such that a patient continues to gain weight with a decline in linear height ( 100 ). Various endocrine etiologies that one could consider in a patient with excessive weight gain in the setting of slow linear growth: severe hypothyroidism, growth hormone deficiency, and Cushing's disease/syndrome ( 58 , 100 ).
Clinical-Physiology of Pediatric Obesity
It is a well-known fact that early AR(increased BMI) before the age of 5 years is a risk factor for adult obesity, obesity-related comorbidities, and metabolic syndrome ( 101 – 103 ). Typically, body mass index (BMI) declines to a minimum in children before it starts increasing again into adulthood, also known as AR. Usually, AR happens between 5 and 7 years of age, but if it occurs before the age of 5 years is considered early AR. Early AR is a marker for higher risk for obesity-related comorbidities. These obesity-related health comorbidities include cardiovascular risk factors (hypertension, dyslipidemia, prediabetes, and type 2 diabetes), hormonal issues, orthopedic problems, sleep apnea, asthma, and fatty liver disease ( Figure 3 ) ( 9 ).
Figure 3 . Obesity related co-morbidities a in children and adolescents. a, NAFLD, Non-Alcoholic Fatty Liver Disease; SCFE, Slipped Capital Femoral Epiphysis; PCOS, Polycystic Ovary Syndrome; OSA, Obstructive Sleep Apnea.
Clinical Comorbidities of Obesity in Children
Growth and puberty.
Excess weight gain in children can influence growth and pubertal development ( 10 ). Childhood obesity can cause prepubertal acceleration of linear growth velocity and advanced bone age in boys and girls ( 104 ). Hyperinsulinemia is a normal physiological state during puberty, but children with obesity can have abnormally high insulin levels ( 105 ). Leptin resistance also occurs in obese individuals who have higher leptin levels produced by their adipose tissue ( 55 , 106 ). The insulin and leptin levels can act on receptors that impact the growth plates with a resultant bone age advancement ( 55 ).
Adequate nutrition is essential for the typical timing and tempo of pubertal onset. Excessive weight gain can initiate early puberty, due to altered hormonal parameters ( 10 ). Obese children may present with premature adrenarche, thelarche, or precocious puberty (PP) ( 107 ). The association of early pubertal changes with obesity is consistent in girls, and is well-reported; however, data is sparse in boys ( 108 ). One US study conducted in racially diverse boys showed obese boys had delayed puberty, whereas overweight boys had early puberty as compared to normal-weight boys ( 109 ). Obese girls with PP have high leptin levels ( 110 , 111 ). Healthy Lifestyle in Europe by Nutrition in Adolescence (HELENA) is a cross-sectional study and suggested an indirect relationship between elevated leptin levels, early puberty, and cardiometabolic and inflammatory markers in obese girls ( 112 ). Additionally, obese girls with premature adrenarche carry a higher risk for developing polycystic ovary syndrome (PCOS) in the future ( 113 , 114 ).
Obesity is an independent risk factor for obstructive sleep apnea (OSA) in children and adolescents ( 12 , 115 ). Children with OSA have less deleterious consequences in terms of cardiovascular stress of metabolic syndrome when compared to adolescents and adults ( 116 , 117 ). In children, abnormal behaviors and neurocognitive dysfunction are the most critical and frequent end-organ morbidities associated with OSA ( 12 ). However, in adolescents, obesity and OSA can independently cause oxidative systemic stress and inflammation ( 118 , 119 ), and when this occurs concurrently, it can result in more severe metabolic dysfunction and cardiovascular outcomes later in life ( 120 ).
Obesity is related to a clinical spectrum of liver abnormalities such as NAFLD ( 121 ); the most important cause of liver disease in children ( 122 – 124 ). NAFLD includes steatosis (increased liver fat without inflammation) and NASH (increased liver fat with inflammation and hepatic injury). While in some adults NAFLD can progress to an end-stage liver disease requiring liver transplant ( 125 , 126 ), the risk of progression during childhood is less well-defined ( 127 ). NAFLD is closely associated with metabolic syndrome including central obesity, insulin resistance, type 2 diabetes, dyslipidemia, and hypertension ( 128 ).
Obese children are also at risk for slipped capital femoral epiphysis (SCFE) ( 129 ), and sedentary lifestyle behaviors may have a negative influence on the brain structure and executive functioning, although the direction of causality is not clear ( 130 , 131 ).
Clinical Comorbidities of Obesity in Adolescents
Menstrual irregularities and pcos.
At the onset of puberty, physiologically, sex steroids can cause appropriate weight gain and body composition changes that should not affect normal menstruation ( 132 , 133 ). However, excessive weight gain in adolescent girls can result in irregular menstrual cycles and puts them at risk for PCOS due to increased androgen levels. Additionally, they can have excessive body hair (hirsutism), polycystic ovaries, and can suffer from distorted body images ( 134 , 135 ). Adolescent girls with PCOS also have an inherent risk for insulin resistance irrespective of their weight. However, weight gain further exacerbates their existing state of insulin resistance and increases the risk for obesity-related comorbidities such as metabolic syndrome, and type 2 diabetes. Although the diagnosis of PCOS can be challenging at this age due to an overlap with predictable pubertal changes, early intervention (appropriate weight loss and use of hormonal methods) can help restore menstrual cyclicity and future concerns related to childbearing ( 11 ).
Metabolic Syndrome and Sleep Disorders
Metabolic syndrome (MS) is a group of cardiovascular risk factors characterized by acanthosis nigricans, prediabetes, hypertension, dyslipidemia, and non-alcoholic steatohepatitis (NASH), that occurs from insulin resistance caused by obesity ( 136 ). Diagnosis of MS in adults requires at least three out of the five risk factors: increased central adiposity, hypertension, hyperglycemia, hypertriglyceridemia, or low HDL level. Definitions to diagnose MS are controversial in younger age groups, and many definitions have been proposed ( 136 ). This is due to the complex physiology of growth and development during puberty, which causes significant overlap between MS and features of normal growth. However, childhood obesity is associated with an inflammatory state even before puberty ( 137 ). In obese children and adolescents, hyperinsulinemia during puberty ( 138 , 139 ) and unhealthy sleep behaviors increase MS's risk and severity ( 140 ). Even though there is no consensus on diagnosis regarding MS in this age group, when dealing with obese children and adolescents, clinicians should screen them for MS risk factors and sleep behaviors and provide recommendations for weight management.
Social Psychology of Pediatric Obesity in Children and Adolescents
Obese children and adolescents may experience psychosocial sequelae, including depression, bullying, social isolation, diminished self-esteem, behavioral problems, dissatisfaction with body image, and reduced quality of life ( 13 , 141 ). Compared with normal-weight counterparts, overweight/obesity is one of the most common reasons children and adolescents are bullied at school ( 142 ). The consequence of stigma, bullying, and teasing related to childhood obesity are pervasive and can have severe implications for emotional and physical health and performance that can persist later in life ( 13 ).
In adolescents, psychological outcomes associated with obesity are multifactorial and have a bidirectional relationship ( Figure 4 ). Obese adolescents due to their physique may have a higher likelihood of psychosocial health issues, including depression, body image/dissatisfaction, lower self-esteem, peer victimization/bullying, and interpersonal relationship difficulties. They may also demonstrate reduced resilience to challenging situations compared to their non-obese/overweight counterparts ( 9 , 143 – 146 ). Body image dissatisfaction has been associated with further weight gain but can also be related to the development of a mental health disorder or an eating disorder (ED) or disorder eating habits (DEH). Mental health disorders such as depression are associated with poor eating habits, a sedentary lifestyle, and altered sleep patterns. ED or DEH that include anorexia nervosa (AN), bulimia nervosa (BN), binge-eating disorder (BED) or night eating syndrome (NES) may be related to an individual's overvaluation of their body shape and weight or can result during the treatment for obesity ( 147 – 150 ). The management of obesity can place a patient at risk of AN if there is a rigid focus on caloric intake or if a patient overcorrects and initiates obsessive self-directed dieting. Healthcare providers who primarily care for obese patients, usually give the advice to diet to lose weight and then maintain it. However, strict dieting (hypocaloric diet), which some patients may later engage in can lead to an eating disorder such as anorexia nervosa ( 151 ). This behavior leads to a poor relationship with food, and therefore, adolescents perseverate on their weight and numbers ( 152 ).
Figure 4 . Bidirectional relationship of different psychological outcomes of obesity.
Providers may not recognize DEHs when a morbidly obese patient loses the same weight as a healthy weight individual ( 149 ). It may appear as a positive result with families and others praising the individual without realizing that this youth may be engaging in destructive behaviors related to weight control. Therefore, it is essential to screen regarding the process of how weight loss was achieved ( 144 , 150 ).
Support and attention to underlying psychological concerns can positively affect treatment, overall well-being, and reduce the risk of adult obesity ( 150 ). The diagram above represents the complexity of the different psychological issues which can impact the clinical care of the obese adolescent.
Eating family meals together can improve overall dietary intake due to enhanced food choices mirrored by parents. It has also may serve as a support to individuals with DEHs if there is less attention to weight and a greater focus on appropriate, sustainable eating habits ( 148 ).
Prevention and Anticipatory Guidance
It is essential to recognize and provide preventive measures for obesity during early childhood and adolescence ( 100 , 153 , 154 ). It is well-established that early AR is a risk factor for adult obesity ( 66 – 68 ). Therefore, health care providers caring for the pediatric population need to focus on measures such as BMI but provide anticipatory guidance regarding nutritional counseling without stigmatizing or judging parents for their children's overweight/obesity ( 155 ). Although health care providers continue to pursue effective strategies to address the obesity epidemic; ironically, they frequently exhibit weight bias and stigmatizing behaviors. Research has demonstrated that the language that health care providers use when discussing a patient's body weight can reinforce stigma, reduce motivation for weight loss, and potentially cause avoidance of routine preventive care ( 155 ). In adolescents, rather than motivating positive changes, stigmatizing language regarding weight may negatively impact a teen and result in binge eating, decreased physical activity, social isolation, avoidance of health care services, and increased weight gain ( 156 , 157 ). Effective provider-patient communication using motivational interviewing techniques are useful to encourage positive behavior changes ( 155 , 158 ).
Anticipatory guidance includes educating the families on healthy eating habits and identifying unhealthy eating practices, encouraging increased activity, limiting sedentary activities such as screen time. Lifestyle behaviors in children and adolescents are influenced by many sectors of our society, including the family ( Figure 1 ) ( 3 , 24 ). Therefore, rather than treating obesity in isolation as an individual problem, it is crucial to approach this problem by focusing on the family unit. Family-based multi-component weight loss behavioral treatment is the gold standard for treating childhood obesity, and it is having been found useful in those between 2 and 6 years old ( 150 , 159 ). Additionally, empowering the parents to play an equal role in developing and implementing an intervention for weight management has shown promising results in improving the rate of obesity by decreasing screen time, promoting healthy eating, and increasing support for children's physical activity ( 160 , 161 ).
When dietary/lifestyle modifications have failed, the next option is a structured weight -management program with a multidisciplinary approach ( 15 ). The best outcomes are associated with an interdisciplinary team comprising a physician, dietician, and psychologist generally 1–2 times a week ( 15 , 162 ). However, this treatment approach is not effective in patients with severe obesity ( 122 ). Although healthier lifestyle recommendations for weight loss are the current cornerstone for obesity management, they often fail. As clinicians can attest, these behavioral and dietary changes are hard to achieve, and all too often is not effective in patients with severe obesity. Failure to maintain substantial weight loss over the long term is due to poor adherence to the prescribed lifestyle changes as well as physiological responses that resist weight loss ( 163 ). American TV hosts a reality show called “The Biggest Loser” that centers on overweight and obese contestants attempting to lose weight for a cash prize. Contestants from “The Biggest Loser” competition, had metabolic adaptation (MA) after drastic weight loss, regained more than they lost weight after 6 years due to a significant slow resting metabolic rate ( 164 ). MA is a physiological response which is a reduced basal metabolic rate seen in individuals who are losing or have lost weight. In MA, the body alters how efficient it is at turning the food eaten into energy; it is a natural defense mechanism against starvation and is a response to caloric restriction. Plasma leptin levels decrease substantially during caloric restriction, suggesting a role of this hormone in the drop of energy expenditure ( 165 ).
The role of pharmacological therapy in the treatment of obesity in children and adolescents is limited.
Orlistat is the only FDA approved medication for weight loss in 12-18-year-olds but has unpleasant side effects ( 166 ). Another medicine, Metformin, has been used in children with signs of insulin resistance, may have some impact on weight, but is not FDA approved ( 167 ). The combination of phentermine/topiramate (Qsymia) has been FDA approved for weight loss in obese individuals 18 years and older. In studies, there has been about 9–10% weight loss over 2 years. However, caution must be taken in females as it can lead to congenital disabilities, especially with use in the first trimester of pregnancy ( 167 ).
GLP-1 agonists have demonstrated great success in effective weight loss and are approved by the FDA for adult obesity ( 168 – 170 ). A randomized control clinical trial recently published showed a significant weight loss in those using liraglutide (3.0 mg)/day plus lifestyle therapy group compared to placebo plus lifestyle therapy in children between the ages of 12–18 years ( 171 ).
Recently during the EASL conference, academic researchers and industry partners presented novel interventions targeting different gut- liver axis levels that include intestinal content, intestinal microbiome, intestinal mucosa, and peritoneal cavity ( 47 ). The focus for these therapeutic interventions within the gut-liver axis was broad and ranged anywhere from newer drugs protecting the intestinal mucus lining, restoring the intestinal barriers and improvement in the gut microbiome. One of the treatment options was Hydrogel technology which was shown to be effective toward weight loss in patients with metabolic syndrome. Hydrogel technology include fibers and high viscosity polysaccharides that absorb water in the stomach and increasing the volume, thereby improving satiety ( 47 ). Also, a clinical trial done in obese pregnant mothers using Docosahexaenoic acid (DHA) showed that the mothers' who got DHA had children with lower adiposity at 2 and 4 years of age ( 172 ). Recently the role of probiotics in combating obesity has emerged. Probiotics are shown to alter the gut microbiome that improves intestinal digestive and absorptive functions of the nutrients. Intervention including probiotics may be a possible solution to manage pediatric obesity ( 173 , 174 ). Additionally, the role of Vitamin E for treating the comorbidities of obesity such as diabetes, hyperlipidemia, NASH, and cardiovascular risk, has been recently described ( 175 , 176 ). Vitamin E is a lipid- soluble compound and contains both tocopherols and tocotrienols. Tocopherols have lipid-soluble antioxidants properties that interact with cellular lipids and protects them from oxidation damage ( 177 ). In metabolic disease, certain crucial pathways are influenced by Vitamin E and some studies have summarized the role of Vitamin E regarding the treatment of obesity, metabolic, and cardiovascular disease ( 178 ). Hence, adequate supplementation of Vitamin E as an appropriate strategy to help in the treatment of the prevention of obesity and its associated comorbidities has been suggested. Nonetheless, some clinical trials have shown contradictory results with Vitamin E supplementation ( 177 ). Although Vitamin E has been recognized as an antioxidant that protects from oxidative damage, however, a full understanding of its mechanism of action is still lacking.
Bariatric surgery has gained popularity since the early 2000s in the management of severe obesity. If performed earlier, there are better outcomes for reducing weight and resolving obesity-related comorbidities in adults ( 179 – 182 ). Currently, the indication for bariatric in adolescents; those who have a BMI >35 with at least one severe comorbidity (Type 2 Diabetes, severe OSA, pseudotumor cerebri or severe steatohepatitis); or BMI of 40 or more with other comorbidities (hypertension, hyperlipidemia, mild OSA, insulin resistance or glucose intolerance or impaired quality of life due to weight). Before considering bariatric surgery, these patients must have completed most of their linear growth and participated in a structured weight-loss program for 6 months ( 159 , 181 , 183 ). The American Society for Metabolic and Bariatric Surgery (AMBS) outlines the multidisciplinary approach that must be taken before a patient undergoing bariatric surgery. In addition to a qualified bariatric surgeon, the patient must have a pediatrician or provider specialized in adolescent medicine, endocrinology, gastroenterology and nutrition, registered dietician, mental health provider, and exercise specialist ( 181 ). A mental health provider is essential as those with depression due to obesity or vice versa may have persistent mental health needs even after weight loss surgery ( 184 ).
Roux-en-Y Gastric Bypass (RYGB), laparoscopic Sleeve Gastrectomy (LSG), and Gastric Banding are the options available. RYGB and LSG currently approved for children under 18 years of age ( 166 , 181 , 185 ). At present, gastric banding is not an FDA recommended procedure in the US for those under 18y/o. One study showed some improvements in BMI and severity of comorbidities but had multiple repeat surgeries and did not believe a suitable option for obese adolescents ( 186 ).
Compared to LSG, RYGB has better outcomes for excess weight loss and resolution of obesity-related comorbidities as shown in studies and clinical trials ( 183 , 184 , 187 ). Overall, LSG is a safer choice and may be advocated for more often ( 179 – 181 ). The effect on the Gut-Brain axis after Bariatric surgery is still inconclusive, especially in adolescents, as the number of procedures performed is lower than in adults. Those who underwent RYGB had increased fasting and post-prandial PYY and GLP-1, which could have contributed to the rapid weight loss ( 185 ); this effect was seen less often in patients with gastric banding ( 185 ). Another study in adult patients showed higher bile acid (BA) subtype levels and suggested a possible BA's role in the surgical weight loss response after LSG ( 188 ). Adolescents have lower surgical complication rates than their adult counterparts, hence considering bariatric surgery earlier rather than waiting until adulthood has been entertained ( 180 ). Complications after surgery include nutritional imbalance in iron, calcium, Vitamin D, and B12 and should be monitored closely ( 180 , 181 , 185 ). Although 5-year data for gastric bypass in very obese teens is promising, lifetime outcome is still unknown, and the psychosocial factors associated with adolescent adherence post-surgery are also challenging and uncertain.
Obesity in childhood and adolescence is not amenable to a single easily modified factor. Biological, cultural, and environmental factors such as readily available high-density food choices impact youth eating behaviors. Media devices and associated screen time make physical activity a less optimal choice for children and adolescents. This review serves as a reminder that the time for action is now. The need for interventions to change the obesogenic environment by instituting policies around the food industry and in the schools needs to be clarified. In clinical trials GLP-1 agonists are shown to be effective in weight loss in children but are not yet FDA approved. Discovery of therapies to modify the gut microbiota as treatment for overweigh/obesity through use of probiotics or fecal transplantation would be revolutionary. For the present, ongoing clinical research efforts in concert with pharmacotherapeutic and multidisciplinary lifestyle programs hold promise.
AK, SL, and MJ contributed to the conception and design of the study. All authors contributed to the manuscript revision, read, and approved the submitted version.
Conflict of Interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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Keywords: obesity, childhood, review (article), behavior, adolescent
Citation: Kansra AR, Lakkunarajah S and Jay MS (2021) Childhood and Adolescent Obesity: A Review. Front. Pediatr. 8:581461. doi: 10.3389/fped.2020.581461
Received: 08 July 2020; Accepted: 23 November 2020; Published: 12 January 2021.
Copyright © 2021 Kansra, Lakkunarajah and Jay. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Alvina R. Kansra, firstname.lastname@example.org
This article is part of the Research Topic
Pediatric Obesity: From the Spectrum of Clinical-Physiology, Social-Psychology, and Translational Research
Causes of Obesity
Food, activity, and sleep, social determinants of health (sdoh), illnesses and medications, what can be done.
Obesity is a complex disease that occurs when an individual’s weight is higher than what is considered healthy for his or her height. Obesity affects children as well as adults. Many factors can contribute to excess weight gain including eating patterns, physical activity levels, and sleep routines. Social determinants of health , genetics, and taking certain medications also play a role.
Eating and physical activity patterns, insufficient sleep and several other factors influence excess weight gain.
The conditions in which we live, learn, work, and play are called social determinants of health (SDOH). It can be difficult to make healthy food choices and get enough physical activity if these conditions do not support health. Differences in SDOH affect chronic disease outcomes and risks, including obesity, among racial, ethnic, and socioeconomic groups as well as in different geographies and among people with different physical abilities.
Places such as childcare centers, schools, or communities affect eating patterns and activity through the foods and drinks they offer and the physical activity opportunities they provide. Other community factors that influence obesity include the affordability of healthy food options, peer and social supports, marketing and promotion, and policies that determine community design.
Genetic changes in human populations occur too slowly to be responsible for the obesity epidemic. Yet variants in several genes may contribute to obesity by increasing hunger and food intake. Rarely, a specific variant of a single gene (monogenic obesity) causes a clear pattern of inherited obesity within a family.  , 
Some illnesses, such as Cushing’s disease, may lead to obesity or weight gain. Drugs such as steroids and some antidepressants may also cause weight gain. Research continues on the role of other factors such as chemical exposures and the role of the microbiome.
- Healthy eating follows the 2020-2025 Dietary Guidelines for Americans external icon . It emphasizes a variety of vegetables and fruits, whole grains, a variety of lean protein foods, and low-fat and fat-free dairy products. It also limits foods and beverages with added sugars, solid fats, or sodium. See Healthy Eating for Healthy Weight .
- Managers of worksites and public facilities can improve the nutritional quality of food and beverages available in those settings. See Food Service Guidelines Implementation Toolkit .
- Physical Activity
- The Physical Activity Guidelines for Americans external icon recommends that children aged 3 through 5 years should be physically active throughout the day. Children aged 6 – 17 years need at least 60 minutes of moderate to vigorous physical activity every day. Adults need 150 minutes of moderate intensity physical activity a week. See Physical Activity for Different Groups .
- Communities can create or modify environments to make it easier for people to walk or bike to everyday destinations. See Community Strategies .
- Newborns need 14 to 17 hours of sleep per day. That amount decreases with age; teenagers need 8 to 10 hours of sleep per day, and adults need 7 or more hours of sleep per day. See How Much Sleep Do I Need?
Social Determinants of Health
- State early care and education systems can promote standards that address nutrition, infant feeding, physical activity, and screen time. See Early Care and Education .
- Communities, programs, initiatives, and public health practitioners can work to together to remove barriers to health and achieve health See Health Equity Resources .
- Bouchard C. Defining the genetic architecture of the predisposition to obesity: a challenging but not insurmountable task external icon . Am J Clin Nutr 2010; 91:5-6.
- Choquet H, Meyre D. Genetics of obesity: what have we learned? external icon Curr Genomics . 2011;12:169-79.
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Writing help, paraphrasing tool, childhood obesity – causes and potential long-term effects.
- Childhood , Childhood Obesity , Food , Healthy Diet , Obesity
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There is growing concern about the state of children’s health. Every year there is an increase in the number of overweight and obese children. What causes this and what does it mean for them long-term? There are many contributing factors to children’s weight issues. Some of these factors are limited access to healthy food, more time spent in front of a screen, and less physical activity. Long-term health affects include a rising risk of Type 2 diabetes, coronary heart disease, and some forms of cancer. The implications are that children are becoming unhealthier every year which raise the cost of medical care and reduce their life expectancy.
Causes and potential long-term effects.
- The causes of childhood obesity
- The cost of medical treatment of childhood obesity and its attendant long-term effects
- The long-term effects of childhood obesity
- Potential solutions for the treatment and prevention of childhood obesity
With an understanding of these areas, we can hope to find solutions that will help current and future generations deal with this growing trend. Childhood obesity effects every area of that child’s life and will continue to affect that child as he or she grows to adulthood.
Causes of Childhood Obesity
There are several causes of childhood obesity from genetics, to a lifestyle of convenience, to ease of access in acquiring healthy foods, among others. While the causes of obesity based on genetics is still being studied, there is some evidence that genetics play a role in childhood obesity. According to Sahoo et al. (2015) “Some studies have found that BMI is 25-40% heritable.” Unfortunately, this means that some children are predisposed to having a higher BMI. They go on to say only 5% of childhood obesity cases can be attributed to this genetic factor and that “Females are more likely to be obese as compared to males, owing to inherent hormonal differences.” These hormonal differences can also be genetically passed down from mother to daughter and father to son.
Another area for concern, in terms of childhood obesity, is the lifestyle of convenience. It is far easier for people to find food in this day and age. Glenn Berall, in his article Obesity: A crisis of growing proportions states that “Never before in the history of civilization has a population had such plentiful food sources without interruption of famine” (2002). This may have led some children to develop a “thrift metabolism” states Rolland-Cachera et al. (2006). A thrifty metabolism is the theory that thrifty genes allow for the storage of food as fat that the body can then use during a famine to continue to give needed energy to the individual. This could explain some of the obesity epidemic as there is rarely ever a famine in this abundant food culture. The lifestyle of convenience goes past readily available to food to available food choices. During the times of hunter-gatherers, food was hard to come by and was considered, by today’s standards, to be healthy. There were no sugary, fatty foods available to these people. They ate what they could find, such as berries, roots, and meat that they caught or killed. Today the food choices are overwhelming. One can simply drive to McDonald’s on the way home to pick up dinner for the family rather than spending time at the grocery store buying healthier options then going home to prepare the meal. In the increasingly busy lifestyle convenience has become the norm, not the atypical go-to for meals.
However, it needs to be mentioned that healthy food is not always easily available to certain demographics. Ashlesha Datar (2017) states that disadvantaged families have higher obesity rates. According to Howlett, Davis, and Burton (2014), “the majority of food deserts in the U.S. are found in low-income neighborhoods.” They state that “food deserts” are areas without “immediate access to fresh, healthy, and affordable food.” There is a high percentage of convenience stores in these areas and a lack of grocery stores or supercenters that would allow for the purchase of healthy foods. Howlett, Davis, and Burton (2014) go on to say:
“only 5 to 10% of convenience stores had fresh produce. In addition, the top selling food items sold at convenience stores include energy-dense foods such as sweet snacks, candy/gum/mints, and salty snacks.”
They continue on to compare the cost of meals. They estimate that it costs roughly $18.16 per 1000 calories for low-calorie meals compared to the $1.76 per 1000 calories of high-calorie foods. This makes it more expensive for low income families to eat healthier and thus could contribute to the rising rates of childhood obesity.
Along with convenience, comes a sedentary lifestyle. Children spend more time in front of a screen, whether it be television, tablet, computer, or phone, than in the past. This leads to less physical activity. Every hour of television a day increases the risk of obesity by 2% (Sahoo et al. 2015). According to the CDC (2017), “Energy imbalance is a key factor behind the high rates of obesity seen in the United States and globally.” Children are consuming more calories today than ever before but are not getting the needed activity to burn those extra calories. This creates a positive energy balance which leads to the storage of excess energy as fat. Convenience extends beyond food. Some of these contributing trends are the increased use of vehicles, more hazards for cyclists and walkers, increased food and drink choices, and media promotion of energy-dense foods (Lobstein et al. 2004).
Rising Cost of Medical Care
Childhood obesity has contributed to the rising cost of health care. Statistically, children who are obese will remain obese in adulthood. This creates the need for long-term medical treatment for a variety of issues. Long-term medical costs for a single obese child come in at approximately $12,660 per year according to Finkelstein et al (2014). In their article, medical for males ranged from $9,640 to $38, 680 with a mean of $24,160. Medical for females ranged from $14,440 to $49,230 with a mean of $31,835. However, some of these numbers do not account for weight fluctuations over a lifetime. By accounting for the fluctuations, they came to an approximate amount of $12,660 a year for both sexes and across each demographic. What time means long-term is that children are obese will pay, on average, more medical expenses than a person who becomes obese as an adult.
Long-Term Effects of Childhood Obesity
There is some controversy over the long-term effects of childhood obesity. Some studies show very little long-term effects while others show an astounding number of effects. However, there are some undisputed long-term risks involved with childhood obesity. Park, Falconer, Viner, and Kinra (2012) have compiled a list of six potential long-term risks associated with childhood obesity. These risks are:
- Type 2 Diabetes
- All-cause mortality
They state that the higher the BMI (body mass index) of the child the greater the risk of developing one or more of the above diseases. “There is a consistent body of evidence for associations between childhood overweight and cardiovascular outcomes and mortality in adulthood” (Park et al. 2012).
Other studies have listed even more potential health problems for obese children. Glenn Berall (2002) lists “sleep apnea, slipped capital femoral epiphyses, nonalcoholic steatohepatitis, polycystic ovarian disease, and metabolic syndrome” as potential problems for overweight children as the reach maturity. Sahoo et al. (2015) list vitamin deficiencies as a current and potential long-term problem for obese children.
What one must also consider is the emotional ramifications of childhood obesity. Sahoo et al. (2015) looked at the relationship between eating disturbances and psychological effects on obese children. They found that obese children are more likely to suffer from self-esteem issues, body dissatisfaction, depression and anxiety, and eating disorder symptoms. They continue on to say that “Childhood obesity effects children’s and adolescent’s social and emotional health.” Overweigth children are more likely to be bullied or teased due to their weight. They are also more likely to be discriminated against. “These negative social problems contribute to low self-esteem, low self-confidence, and a negative body image in children and can also affect academic performance” (Sahoo et al. 2015).
What can society do to help treat or prevent childhood obesity? There are several things that society can do including changing governmental policies on food distribution and promotion, promote healthier food choices at schools, and advocate for healthier food options in the media.
Governmental policies could create incentives for schools to promote healthier food options. If a school is willing to participate, there could be a financial advantage to that school so that they could help offset the cost of healthier food. The government could offer incentives to grocery stores to build in low-income neighbors to help provide better food options to low-income families. They could also create policies aimed at the media to promote healthy food over junk food.
The media could promote healthier food options and more realistic body ideals. This would help with the perception that all women must be skinny and all men must be buff which create an unrealistic ideal for children to live up and may contribute to increased eating.
There are several contributing factors to why childhood obesity rates have grown exponentially over the last 40 years. A sedentary and convenient lifestyle, increased access to all types of food, and genetics all play a role. These can lead to long-term habit creation, as in the lack of consistent physical activity and eating a high fat diet, as well as long-term health effects such as Type 2 diabetes, heart disease, and increased risk of cancer. Childhood obesity also leads to higher long-term medical and emotional costs. Change needs to become a priority. The government, media, and schools need to lead the charge in promoting healthier food and education on the long-term risk factors associated with childhood obesity. Change won’t happen overnight, but it can happen.
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Home — Essay Samples — Nursing & Health — Childhood Obesity — The Main Causes Of Childhood Obesity: Child’s Environment
The Main Causes of Childhood Obesity: Child's Environment
- Categories: Child Obesity Childhood Obesity Obesity
About this sample
- Berall, G. (2002). Walking to school: a step to healthy children. Canadian Medical Association Journal, 166(3), 322-323.
- Ogden, C. L. (2011). Genetics of childhood obesity. Pediatrics, 128(Supplement 2), S152-S155.
- Rosenfield, S. (2007). Perspectives on the prevention and treatment of childhood obesity. Journal of School Health, 77(3), 124-128.
- Sahoo, K., Sahoo, B., Choudhury, A. K., Sofi, N. Y., Kumar, R., & Bhadoria, A. S. (2015). Childhood obesity: causes and consequences. Journal of Family Medicine and Primary Care, 4(2), 187-192.
- Singh, A. S., Mulder, C., Twisk, J. W., van Mechelen, W., & Chinapaw, M. J. (2008). Tracking of childhood overweight into adulthood: a systematic review of the literature. Obesity Reviews, 9(5), 474-488.
- Swinburn, B. A., Sacks, G., Hall, K. D., McPherson, K., Finegood, D. T., Moodie, M. L., & Gortmaker, S. L. (2011). The global obesity pandemic: shaped by global drivers and local environments. The Lancet, 378(9793), 804-814.
- U.S. Department of Health and Human Services. (2018). Physical Activity Guidelines for Americans, 2nd Edition. U.S. Department of Health and Human Services. https://health.gov/our-work/physical-activity/current-guidelines
- Vogels, N., Posthumus, D. L., Marang-van de Mheen, P. J., & Renders, C. M. (2018). Behavioral factors related to the development of healthy and unhealthy habits in overweight preschool children: a cross-sectional study. International Journal of Behavioral Nutrition and Physical Activity, 15(1), 1-9.
- Ward, D. S., Welker, E., Choate, A., Henderson, K. E., Lott, M., Tovar, A., & Wilson, A. (2015). Strength of obesity prevention interventions in early care and education settings: A systematic review. Preventive Medicine, 78, 23-33.
- Whitaker, R. C., Wright, J. A., Pepe, M. S., Seidel, K. D., & Dietz, W. H. (1997). Predicting obesity in young adulthood from childhood and parental obesity. New England Journal of Medicine, 337(13), 869-873.
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Causes and Effects of Childhood Obesity: a Comprehensive Approach
Over the previous decades, youth fatness has been at a constant increase. Youth chubbiness is an emerging issue in the United States. Everywhere you look, there are millions of advertisements for fast, and deep fried foods. This appeals to young minds because it tastes scrumptious. As young children, they do not generally think about how these foods will affect their bodies in the long run. This exploration will present that youth obesity roots from the monetary remaining of the family, depends on the race/ethnic foundation, and relies upon how persuasive the parents are towards their children eating habits. With the end goal to avert childhood obesity, there should be a program that educates kids and their parents on the results of unfortunate eating patterns.
Different sources have diverse perspectives regarding the matter of childhood obesity including, race and ethnics, the role of parents, as well of the measure of a child’s body mass index (BMI). Davis- Kean’s whole approach in “Race/ethnic disparities in early childhood BMI, obesity and overweight in the United Kingdom and United States” roots from race and ethnics. He argues that dependent on somebody's race and ethnicity it can be determined whether or not they will be influenced by childhood obesity. He backs up his contention by saying, “Some studies suggest that racial/ ethnic minority children from households with low income and whose parents have low educational attainment may be less likely to be overweight than their socioeconomically advantaged minority counterparts” (Davis-Kean, 2015, p. 520). Next, Barry states in his article, “The Role of Parents in Public Views of Strategies to Address Childhood Obesity in the United States”that parents are the sole fault of youth obesity. In his policy points, toward the start of his discoveries, he states, “The American public- both with and without children in the household- holds parents highly responsible and largely to blame for childhood obesity” (Barry, 2015, p.73).He isn't attempting to sound condescending in any case, he wants to recognize that parents need to make the initial step to changing their kid’s way of life to avoid any future medical problems. Kimm chooses not to depend on fault and rather utilizes the research in “Childhood Obesity: A New Pandemic of the New Millennium”. She first relates race and gender to the percentile of body mass index (BMI). She says, “Based on National Health Examination Survey’s BMI information, childhood obesity was about one third higher in black girls than in white girls- 31% versus 22%” (Kimm, 2002, p. 1003). Kimm goes on to use race, but takes a different approach than Davis-Kean. She says, “…more of the thin black girls than white girls reported trying to gain weight, suggesting a low tolerance by black girls for being too thin (Kimm, 2002, p. 1004). This immediate statement demonstrates the understanding of psychological factors behind youth obesity. Studies demonstrated that regardless of how much weight a Caucasian young lady lost, she was as yet troubled with her body weight and body shape. African American girls in the study demonstrated that they lean more towards being somewhat more 'curvy' and embrace a portion of the weight in the right spots. She goes on to say, “Nine- and 10- year old black girls were more than twice as likely as white girls to engage in less favorable eating practices, such as eating big helpings (Kimm, 2002, p. 1004).These four sources likewise have a variety of ideas. Although a few points are similar, they also contrast. Some of the sources corroborate with one another to demonstrate the arguments. Kimm and Davis-Kean agree on BMI research. Kimm (2002) says, “BMI… was about one third higher in black girls than in white girls- 31% versus 22%” (p. 1003). Davis-Kean (2015) agrees with statistics in a chart titled “Children’s BMI and obesity… by race/ ethnicity” (p. 524).In this chart, he arranges kid’s fatness by race/ethnicities. Caucasian children have a BMI of about 16.40 and an obesity rate of about 11.3 %, whereas African American children have a BMI of approximately 16.66 and an obesity rate roughly at 13.5% (Davis-Kean, 2015, p.524).Davis-Kean’s graph additionally substantiates with Barry’s second table. Davis-Kean (2015) has a graph that says that Hispanics with less than a high school diploma are in the least in heftiness contrasted with different Hispanics with various diplomas and/or degrees (p. 524). Barry (2015) says that Hispanic parents and their kids with less than a high school diploma have an obesity rate of about 11.8%- which is lower than others that have achieved more (p. 82). Lastly, Davis-Kean and Kimm concur that a family's financial position is a factor in obesity. Davis-Kean (2015) depicts this in a circle graph that rundowns financial position, socio-statistic characteristics, parenting strategies, family eating times, and social area all factors that can lead or avoid obesity (p. 521). Kimm firmly agrees with this. She states, “Poverty has often been considered a major contributor to the high prevalence of obesity seen in children in the U.S.” (Kimm, 2002, p. 1004). Dr. Al Gilpin states in his article, “Childhood Obesity: Why Worry?” that children who are obese often suffer from depression and bullying. This article focuses on the medical effects on children. “Extra weight can have a devastating impact on children, causing them to suffer joint, leg, and back pain when instead they should be playing torment free” (Gilpin, 2017).
All together for children and their parents to completely get a handle on the concept of youth obesity, there should be programs that legitimately teach them on the impacts of unfortunate eating habits. The program would incorporate classes for the parents and intuitive recreations for the kids.The reasoning behind that would be because adults have enough control to sit through presentations and bring down valuable tips and really utilize the information. Youthful children generally like to be energetic and more involved. Their capacity to focus isn't sufficiently long to sit through educational meetings. I hypothesize if these programs were held for little to zero cost or even free, youth stoutness rates would drop hugely. By removing the price factor, anybody will have access to this asset and eventually have the capacity to prolong their life expectancy.
The seminars for the parents would incorporate a day of speakers, a lunch, and an open floor for discussions between parents. The speakers at the seminar would incorporate health care specialists, individuals with past encounters, and the individuals who do inquire about regarding the matter. The speakers will give the parents information to help enhance the family diets and diminishing the level of youth obesity. The lunch accommodated them would incorporate solid alternatives. Things that are simple and quick to cook at home. For example, grilled or baked chicken breast, broccoli, brown rice, squash, and whatever else that can be boiled.
For kids, their interactive exercises would incorporate craft, fun, healthy recipes to make with parents, and exercise. The crafts could be motivational self-portraits or posters. The healthy recipes that the children find would be for kids to have a ton of fun in the kitchen with their parents making nourishment they love! The activity would incorporate running, bicycle riding, playing tag, and additionally extraordinary group activities, for example, b-ball and football. This would enable the children to figure out how to cherish physical movement.
The whole program would be each end of the week for an entire three weeks. It would just be on weekends to oblige the accessibility of the parents and children. Parents have a wild work day and need to loosen up when they return home. Children have school and homework when they return home. The mission of this program is to the parents and their kids 'homework' for the week. The homework is actualizing every one of the tips given to them at the meetings. They would then report back and state what was effective and what was most certainly not. And in addition what will work in their family and what won't.
In conclusion, youth obesity has a simple solution. Research has discovered that parents and children need to work together in order to fight the annoying weight problem. Kids can't fit this issue independently from anyone else. They need the parents to take the first step. The seminar and interactive exercises are the initial step to accomplishing this. By taking the first step, children will be more willing to follow in their parent’s footsteps.
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Causes and Effects of Childhood Obesity: A Comprehensive Approach. (2021, Apr 19). Retrieved from https://studydriver.com/essay-on-childhood-obesity/
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7 common causes of childhood obesity to look out for
Posted: November 6, 2023 | Last updated: November 6, 2023
Childhood obesity has grown into a severe issue that affects children all over the world. Obesity is a severe medical condition affecting kids and teens just like adults. It's particularly concerning because the extra pounds frequently set children on a trajectory to medical conditions that used to be adult problems-diabetes, elevated blood pressure, and high cholesterol.
Childhood obesity has ramifications beyond physical health. Children and adolescents who are overweight or obese may experience depression and have a negative self-image and self-esteem.
10 causes of childhood obesity
The biggest reason for childhood obesity is unhealthy lifestyle choices. Childhood obesity can, however, be caused by hereditary and hormonal causes. The following are some of the primary causes of childhood obesity:
There are numerous causes of medication-related weight gain. Many medicines tend to make you feel hungry. It also leads you to overeat and gain weight. Some medications may affect your body's metabolism.
This causes you to weigh more, even though you don't gain weight. Other medications could have an impact on how the human body accumulates and absorbs carbohydrates and other nutrients.
Type 2 diabetes is a disorder that occurs when your body cannot efficiently metabolize glucose. Diabetes can cause severe problems, including
- Kidney Failure
- Nerve damage
Overweight children and adults are more likely to develop type 2 diabetes . The illness, however, may be treatable via dietary and lifestyle modifications.
3) Socioeconomic factors
Certain childhood obesity risk factors, such as residing in a low-income neighborhood and surroundings could mean that there is a lack of availability of fresh vegetables and fruits.
As a result, such societies are compelled to consume an excessive quantity of carbs and processed foods in comparison to a healthy, low-calorie diet.
Obesity in children can be predisposed to by genetic factors . Children who have obese parents or siblings are more likely to develop the illness themselves.
Various genes have been linked to weight gain in studies. Although obesity runs in families, not every kid with a family history of obesity will become obese.
5) Sleep disorders
Sleep deprivation has been shown in studies to increase appetite and lead to overeating, most likely due to the impact on hormones that associate hunger and fullness.
Furthermore, studies have shown that a lack of sleep might boost your preference for foods heavy in carbs, calories, and fat. Those who get sufficient restful sleep are likely to eat fewer calories compared to those who don't.
Consuming high-calorie foods, such as baked goods and processed foods, may affect children and be a major cause of their being overweight. Eating too many sweets or chocolates may also raise the likelihood of children developing diabetes.
7) Lack of exercise
In addition to outdoor activities, children always desire to spend time on television, use their cell phones, or enjoy video games. This practice may also enhance the likelihood of being overweight.
If you have concerns that your child may be obese, speak with their doctor. Their provider can help you determine whether the weight of your child is concerning. They can help you devise a plan to get your family and friends back on track with healthier eating and more strenuous physical activity.
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