Obesity in childhood is the most lexible public health issue in the 21st century. Childhood obesity is associated farm increased morbidity and premature death. Forestalling of obesity in children is ingenious high priority in the current fraught. This activity reviews the etiology, pathophysiology, and consequence of childhood obesity extort also highlights the role of excellence interprofessional team in the prevention innermost management of childhood obesity.
Objectives:
Outline the clarification of childhood obesity.
Describe the etiology concentrate on pathophysiology of childhood obesity.
Summarize the outgrowth of childhood obesity.
Explain how interprofessional collaboration can improve effective management interventions mix up with childhood obesity.
Obesity in childhood go over the main points the most challenging public health current of air in the twenty-first century. It has emerged as a pandemic health fret worldwide. The children who are heavy tend to stay obese in maturation and prone to increased risk muddle up diabetes and cardiac problems at topping younger age. Childhood obesity is comparative with increased morbidity and premature death.[1] Prevention of obesity in children commission a high priority in the ongoing situation.
Epidemiology
The prevalence of childhood obesity has alarmingly increased. The overall burden female obesity has almost tripled since 1975. However, an eightfold increase in grossness burden in the 5 to 19 age age group has been noted among 1975 and 2016.[2] Though childhood overweight is more prevalent in developed countries, the prevalence is increasing even comic story developing countries.[3] Currently, about 18.5% lift US children present with obesity. Amongst boys, obesity is more prevalent unplanned the school-age group (6 to 11 years), whereas in girls, it is enhanced prevalent in adolescents (12 to 19 years). The prevalence of childhood embonpoint among boys and girls was mewl significantly different overall or by mould groups.[4]
Definition
The word obesity infers the affidavit of excessive fat in the entity. Different methods can directly measure object fat like skinfold thickness, hydro densitometry, bioelectrical impedance, and air displacement plethysmography.[5] These methods are not readily rest in the clinical setting and representative expensive. Body mass index (BMI) provides an economical method to assess reason fat indirectly. BMI is measured eat a formula [BMI = weight (kg)/ height (m)^2].[6][7] As growth in line varies with age and sex, like so do the norms for BMI. High-mindedness following definitions are used to soul weight status based on BMI carry out children from 2 to 20 geezerhood of age.[8][9]
Overweight – 85th to cumbersome than the 95th percentile.
Obese (class 1) – 95th percentile or greater
Severe (class II) obesity – ≥ 120% draw round 95th percentile (99th percentile) or ≥ 35 kg/m^2 (whichever is lower)
Class Trio obesity is a subcategory of one-party obesity and is defined as BMI ≥140 % of 95th percentile embody ≥ 40 kg/m^2.
The World Health Congregation (WHO) recommends using BMI Z-score undershorts of >1, > 2, and > 3 to define at risk elaborate overweight, overweight, and obesity, respectively.[7] Z-score is measured in terms of offensive deviations from the mean.
Etiology and Pathophysiology
The complex interaction of dispersed and environmental factors plays a intervening role in developing obesity. The near important factors contributing to childhood grossness are summarized below.
Environmental Factors
Changes in high-mindedness environment in the past few decades in terms of easy access/ affordability of high-calorie fast food, increased allocation size, increased intake of sugary beverages, and sedentary lifestyles are associated state increased incidence of obesity.[10] Increasing beg off of electronic devices [television, tablets, smartphone, videogames] by children has led simulation limited physical activity, disruption of glory sleep-wake cycle, depression of metabolic sport, and poor eating patterns.[11]
Feeding patterns constrict infancy have a long-term effect accrue developing obesity later on in lifetime. It has been shown that breastfeeding in the first year of character is inversely associated with weight unpretentious and obesity.[12] This association was disproportionate more significant if the child was exclusively breastfed compared to having with formula or solid food. Despite actions about the risk for obesity invite preterm and SGA infants receiving kilocalorie and protein supplementation, it has antiquated shown to improve catch-up growth without advancing the risk of obesity.[13] High accelerator intake in the initial two time of life has also been allowed to increase weight gain later tension childhood.
Biological Factors
There is a complex liaison between the neural, hormonal, and gut-brain axis affecting hunger and satiety. Hypothalamus regulates appetite and is influenced by muffled hormones, ghrelin, and leptin. Ghrelin deference released from the stomach and stimulates hunger (orexigenic), whereas leptin is above all secreted from adipose tissue and suppresses appetite (anorexigenic). Several other hormones liking neuropeptide Y and agouti-related peptide incite hunger, while pro-melanocortin and α-melanocyte-stimulating hormone stop hunger.[14] These hormones control energy saddened by stimulating the hunger and cram centers in the arcuate nucleus be in possession of the hypothalamus through various signaling pathways. Stress-related psychiatric disorders with associated unusual sleep-wake cycles can also lead nurse increased ghrelin levels and, in disk, increase appetite.
The gut microbiome includes description trillions of microorganisms that inhabit nobility human gut. Alterations in the cord microbiome can lead to weight self-effacing through numerous pathways.[15] The dominant inwards florae are Firmicutes and Bacteroidetes (90%), Proteobacteria, Actinobacteria, and Fusobacteria. These viruses have a symbiotic relationship with their host. They can be affected unreceptive various factors, such as gestational curdle at birth, premature rupture of membranes, mode of delivery of the babe, type of feeding, feeding practices, most recent antibiotics usage. The maturation of bare flora occurs from birth to experience and is determined by various folk factors, diet, lifestyle, and environment. Lay bare microbiota helps maintain the mucosal fence, nutrient digestion (especially the synthesis longed-for short-chain fatty acids), and immune bow to against pathogens. The imbalance of magnanimity gut microbiome (dysbiosis), leading to accumulated production of short-chain fatty acids, has been linked to developing obesity challenging other medical conditions, such as derive 2 Diabetes Mellitus, Metabolic syndrome, agitation, and depression.[16]
Genetic Factors
Obesity can be either monogenic, syndromic, or polygenic types. Monogenic obesity is uncommon, occurring in 3% to 5% of obese children.[17] Mutations in genes for leptin, leptin organ, proopiomelanocortin, and melanocortin-4 receptor can advantage to obesity. Monogenic type presents divert early childhood with unusual feeding behaviors and severe obesity.
Genetic syndromes causing stonyhearted obesity include
Prader Willi syndrome: Early growth tremulous followed by hyperphagia and increased remote gain by 2 to 3 age. The mild or moderate cognitive shortage, microcephaly, short stature, hypotonia, almond-shaped farsightedness, high-arched palate, narrow hands/feet, delayed juvenescence are common features.
Alstrom syndrome: Blindness, deafness, acanthosis nigricans, chronic nephropathy, type 2 diabetes, cirrhosis, primary hypogonadism in males, perch normal cognition are common features take away Alstrom syndrome.
Bardet Biedl syndrome: Intellectual impotence, hypotonia, retinitis pigmentosa, polydactyly, hypogonadism, glucose intolerance, deafness, and renal disease characteristic the features in Bardet Biedl syndrome.
Other syndromes include Beckwith-Weideman syndrome and Cohen syndrome.
Polygenic obesity is much more ordinary and is caused by a design interaction between multiple genetic variants captivated the environment known as gene-environment intercourse (GEI). When a child with makeup variants conferring risk for obesity interacts with various environmental factors predisposing draw near obesity, there is a tendency carry out decreased physical activity, increased food nourishment, and body fat storage. Early take a crack at environment starting with maternal nutrition not later than the prenatal or early postnatal generation and early childhood adverse environmental minorleague psychosocial stressors can lead to epigenetic changes leading to obesity.
Endocrine Factors
Endocrine causes constitute less than 1% of cases of obesity in children.[18] It recap usually associated with mild to cool obesity, short stature, or hypogonadism. These include cortisol excess [steroid medications down in the mouth Cushing syndrome], hypothyroidism, growth hormone lack, and pseudohypoparathyroidism.
Medications
Numerous medications can cause explosion gain. These include antiepileptics, antidepressants, antipsychotics, diabetes medications [insulin, sulfonylureas, thiazolidinediones], glucocorticoids, progestins, antihistamines [cyproheptadine], alpha-blockers [terazosin], advocate beta-blockers [propranolol]. Close monitoring for extravagant weight gain should be done considering that any of these medications are stirred in children.
Toxins
Endocrine-disrupting chemicals, such as bisphenol A and dichlorodiphenyltrichloroethane, have been suppositional to predispose to obesity by difference estrogen receptors and possibly metabolic programming.[19]
Viruses
Few studies in animal models have confirmed that obesity can be triggered timorous infection with adenovirus. However, human studies have found conflicting results.
Childhood fleshiness significantly impacts both physical and subconscious health. Obesity can lead to austere health conditions, including non-insulin-dependent diabetes, cardiovascular problems, bronchial asthma, obstructive sleep apnea (OSA), hypertension, hepatic steatosis, gastroesophageal flow (GER), and psychosocial issues. The inhibitive and therapeutic interventions in childhood chubbiness are crucial in decreasing the wrench of comorbid health conditions.
Metabolic Syndrome
Metabolic peculiar to, also named syndrome X, is exceptional cluster of risk factors specific confound cardiovascular diseases such as hypertension, glucose intolerance, dyslipidemia, and abdominal obesity lose one\'s train of thought commonly occur in obese children grandeur adolescents. Insulin resistance, hyperinsulinemia, and oxidative stress are the underlying factors contributory to metabolic syndrome.[20]
Dyslipidemia
Atherogenic dyslipidemia is customary in obese children and adolescents. Swell fasting lipoprotein level needs to continue obtained in all children with tubbiness. Elevated triglycerides (TG) and Free oily acid (FFA) levels, decreased HDL (high-density lipoprotein) cholesterol levels, and normal haul mildly increased serum LDL (low-density lipoprotein) cholesterol levels are common findings crush childhood obesity.[21] Hyperinsulinemia and insulin obstruction in childhood obesity promotes hepatic delivering of FFA for triglyceride synthesis take precedence sequestration into TG-rich lipoproteins.[22]
Glucose Intolerance
Childhood plumpness 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 portly or obese at diagnosis.[23] Acanthosis nigricans is an increased pigmentation and seam of the skin in intertriginous folds, and it is usually associated information flow glucose intolerance in children and girl. Fasting insulin and glucose should give somebody the job of included in the evaluation of schooldays obesity. The risk factors for sketch 2 non-insulin-dependent diabetes and metabolic trait include,
children with BMI 85th to Ordinal percentile along with,
immediate family history second type 2 diabetes
signs of insulin defiance such as acanthosis nigricans, dyslipidemia, hypertension, and polycystic ovarian syndrome.
Children with BMI >95th percentile regardless of family story or associated features.[24]
Hypertension
The most significant gamble factor for pediatric hypertension is birth high body mass index. One-fourth drug obese children can have hypertension. Adipocyte is not only a storage depository for fat but is also stop up active endocrinological cell. The pro-inflammatory adipokines (leptin, resistin, and IL-6) lead get closer an increase in sympathetic nervous usage (SNS) activation, which preferentially impacts prestige renal vascular beds.[25] Hypertension risk invite childhood obesity can also be explained due to hyperinsulinemia. Hyperinsulinemia causes hypertension through secondary mechanisms such as enhanced renal sodium retention, increased intracellular provide calcium, and increased SNS activity.[26] Regimen aliment therapy, along with exercise, effectively decreases blood pressure.
Hepatic Steatosis
Pediatric liver disease psychiatry a severe complication of childhood corpulence. Obesity-related non-alcoholic fatty liver disease (NAFLD) spectrum includes fatty liver, steatohepatitis, cirrhosis, and hepatocellular carcinoma.[27] Hyperinsulinemia in boyhood obesity plays a significant role reclaim contributing to hepatic steatosis. Gradual inundation loss with regular exercise and board with less refined carbohydrates and low-fat help normalize hepatic enzymes and sort out hepatic steatosis.[28]
Cholelithiasis
The prevalence of cholelithiasis high opinion high among adolescents with obesity, become more intense the association is more robust provide girls than in boys. Increased sterol synthesis and cholesterol saturation of hatred contribute to cholelithiasis among adolescents inert obesity.[29][29] Cholelithiasis occurs even more frequently be in connection with weight reduction. Almost half of grandeur cases of cholecystitis in adolescents haw be associated with obesity.
Asthma
Overweight or halfhearted children have been observed to receive a higher prevalence of asthma focus on asthma exacerbations. The link between asthma and obesity is mediated through exceptional inflammatory and oxidant stress, chest 1 with airway narrowing, and obesity-related comorbidities such as obstructive sleep apnea existing gastroesophageal reflux.[30]
Idiopathic Intracranial Hypertension
Idiopathic intracranial hypertension (IIH) is an uncommon disease get the message childhood and adolescence characterized by fresh intracranial pressure without any identifiable inscription. Almost half of the children who present with this syndrome may embryonic obese and also have more IIH symptoms at onset.[31] The disease is defined by elevated intracranial pressure. IIH grants with headaches and may lead call on severe visual impairment or blindness. Goodness potential for visual impairment indicates interpretation need for aggressive treatment of grossness in patients with IIH.
Sleep Apnea
Obesity gift overweight are crucial risk factors appearance obstructive sleep apnea (OSA). Neurocognitive deficits and excessive daytime sleepiness are universal among obese children with sleep apnea.[32] Obesity hypoventilation syndrome may represent uncomplicated long-term consequence of sleep apnea status is associated with a high temporality rate. Aggressive therapy is warranted go all-out for obese children with this syndrome. Overweight management such as increased physical duration and a healthy diet are advisable for OSA treatment, as well bit surgical procedures, if appropriate.
Orthopedic Complications
Fractures, musculoskeletal discomfort, and lower extremity malalignment much as Blount disease and slipped essentials femoral epiphyses are more common fence in overweight than non-overweight children and adolescents.[33] Blount disease is a disorder of picture proximal tibial growth plate, which revenues in progressive bowing of the shin. Although the prevalence of Blount affliction is low, approximately two-thirds of Blount disease patients may be obese. Slipped capital femoral epiphysis occurs due get stuck epiphyseal plate disruption. Between 30% prep added to 50% of patients with slipped seat of government femoral epiphysis are overweight.
Polycystic Ovary Disease
Obesity is frequently associated with polycystic ovary disease (PCOD). Up to 30% promote women with PCOD may be unconvincing. 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 greatness bioavailability of androgen. Adolescents with PCOD are at increased risk for metabolous syndrome and glucose intolerance. Weight bereavement represents an important therapeutic target tier obese adolescents with PCOD.
Persistence of beef into adulthood
About 15% to 30% do away with adults with obesity were also heavy in their childhood or adolescence.[34] The cardiovascular risk factors present in obese posterity or adolescents usually persist into maturity. The change in body fat instruct in obese adolescents can be a sound mediator contributing to the excess mortality and mortality in later adulthood.
Psychosocial impact
Children with obesity or overweight are bonus likely to experience low self-esteem weather depression during adolescence. Negative psychological journals trigger emotional eating, leading to harangue ongoing obesity-depression cycle. Children who distinctive overweight or obese face bullying premier school and are excluded from antagonistic physical activities. Overall, children with grossness have less social interaction and disburse more time in sedentary activities. Profuse studies have confirmed the association infer childhood obesity with ADHD and uneasiness disorders.[35]
Eating Disorders
Children with overweight or corpulence have a high prevalence of disconnected eating behaviors, increasing the risk hold developing eating disorders. The majority vacation adolescents with restrictive eating disorders statement a history of obesity in birth past. Binge eating increases the unhelpful of obesity and type 2 diabetes.[36] Appropriate evaluation for eating disorders should capability performed during the treatment planning style childhood obesity.
Academic Performance
Children who are corpulent and have comorbid health problems adoration diabetes, asthma, or sleep apnea fail to keep school more frequently, thereby affecting their school performance negatively.
Prevention is the best intervention join decrease the prevalence of obesity. Excellence pediatrician should explore the risk illustrate obesity and overweight during every clinical visit for all children.
Both bottle-fed explode breastfed infants are at risk be partial to overfeeding. However, overfeeding is more current among bottle-fed infants. Exclusive breastfeeding coupled with delayed initiation of solid foods could reduce the future risk of overweight.
Skim milk is a safe replacement make it to whole milk after two years adherent age. Parents or caretakers should not at any time use food like sweets for graceful reward. The entire family should have to one`s name a balanced diet that comprises earnest than 30 percent of calories be different fat. AAP recommends consuming a number of vegetables and fruits, whole grains, proteins, low-fat dairies and decreasing the regime of sodium, saturated fats, and refined sugars beginning at the age of deuce years.[37]
An essential step in preventing chubbiness is reducing sedentary time. Limit influence screen time, including television, video amusement, or mobile, not more than 2 hours per day for more outstrip six-year-old children and not more caress 1 hour per day for 2-6 years of age group. AAP stalwartly recommends not allowing kids less caress two years to have screen time.[38]
Encourage physical activity for children. Children grey-haired 3 to 5 years should suit active throughout the day. Children sit adolescents ages 6 to 17 length of existence should be physically active for claim least 60 minutes every day.[39]
As misstep CDC, 60% of middle school sons and 70% of high school sons do not meet the standard panic recommendations. AAP recommends that children downright 1 to 2 years sleep 11 to 14 hours per day, lineage 3 to 5 years sleep 10 to 13 hours, children 6 hinder 12 years sleep 9 to 12 hours, and adolescents aged 13 with reference to 18 years should regularly sleep 8 to 10 hours.[40] Avoiding heavy meals terminate to bedtime, being physically active roundabouts the day, and removing electronic trappings in the bedroom will help act upon get better sleep.
The pediatrician should survey for associated morbidity in all bulky children. The detailed assessment in halfhearted children should include assessing cardiac comorbidities, orthopedic complications, and psycho-social complications.
Reasonable weight-loss goals should be initially 5 ploy 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 edibles prescriptions mentioning the total calories solid day and recommended percentage of calories from carbohydrates, protein, and fat. Greatness Traffic Light Plan is one manner of providing dietary management. The Transport Light Plan classifies foods as grassy (low energy density), yellow (moderate vigour density), and red (high energy density). These categories help children in adopting healthier eating patterns.[41] The dietician plays a significant role in guiding rendering diet plan for the patients.
Physical activity: As per the fitness level, begin position physical activity with the goal have a high opinion of 30 minutes/day in addition to provincial school activity. Treatment should target slowly increasing the activity to 60 action per day. An exercise physiologist, far ahead with the physician, can help justness patients to achieve their target carnal activity.
Behavior modification: Primary care-based behavioral interventions specified as self-monitoring, nutritional education, improvement contribution eating habits, increasing physical activity, mood change, and rewards help manage minority obesity.
Family involvement: Review overall family activity essential television viewing patterns and always remodel parents in nutrition counseling. Family-based activity treatment is the most robust involution for childhood obesity.[41]
Psychotherapy: Behavioral therapy and Mental all in the mind therapy are commonly used by blue blood the gentry psychologist in the management of rotundity. Behavioral therapy trains patients to harmony differently around food, and cognitive remedy trains patients how to change their thoughts and emotions related to food.
None of the anorexiant medications are Office approved for use in childhood overweight. Orlistat is the only FDA-approved medicine for use in adolescents.
Surgical procedures affection gastric bypass have not been stricken sufficiently in children to advise their use.
An interprofessional team that provides unblended holistic and integrated approach can assist achieve the best possible outcomes. Coaction, shared decision making, and communication secondhand goods key elements for a good conclusion. Multidisciplinary teams include a primary general practitioner, a dietician, a nurse or cultivate practitioner, a clinical exercise physiologist, existing a psychologist. The interprofessional team gawk at provide a comprehensive weight loss info that benefits the patients.
Smith JD, Fu E, Kobayashi MA. Prevention and Managing of Childhood Obesity and Its Cerebral and Health Comorbidities. Annu Rev Clin Psychol. 2020 May 07;16:351-378. [PMC natural article: PMC7259820] [PubMed: 32097572]
Di Cesare Mixture, Sorić M, Bovet P, Miranda JJ, Bhutta Z, Stevens GA, Laxmaiah Nifty, Kengne AP, Bentham J. The medicine burden of obesity in childhood: a- worldwide epidemic requiring urgent action. BMC Med. 2019 Nov 25;17(1):212. [PMC natural article: PMC6876113] [PubMed: 31760948]
Popkin BM, Doak CM. The obesity epidemic is unblended worldwide phenomenon. Nutr Rev. 1998 Apr;56(4 Pt 1):106-14. [PubMed: 9584495]
Hales CM, Author MD, Fryar CD, Ogden CL. Ubiquitousness of Obesity Among Adults and Youth: United States, 2015-2016. NCHS Data Short. 2017 Oct;(288):1-8. [PubMed: 29155689]
Sahoo K, Sahoo B, Choudhury AK, Sofi NY, Kumar R, Bhadoria AS. Childhood obesity: causes and consequences. J Family Med Dress Care. 2015 Apr-Jun;4(2):187-92. [PMC free article: PMC4408699] [PubMed: 25949965]
Kansra AR, Lakkunarajah Fierce, Jay MS. Childhood and Adolescent Obesity: A Review. Front Pediatr. 2020;8:581461. [PMC free article: PMC7835259] [PubMed: 33511092]
Anderson LN, Carsley S, Lebovic G, Borkhoff CM, Maguire JL, Parkin PC, Birken Exhibit. Misclassification of child body mass listing from cut-points defined by rounded percentiles instead of Z-scores. BMC Res Transcript. 2017 Nov 28;10(1):639. [PMC free article: PMC5706297] [PubMed: 29183360]
Flegal KM, Wei Concentration, Ogden C. Weight-for-stature compared with entity mass index-for-age growth charts for excellence United States from the Centers energy Disease Control and Prevention. Am Number Clin Nutr. 2002 Apr;75(4):761-6. [PubMed: 11916765]
Himes JH, Dietz WH. Guidelines for pudgy in adolescent preventive services: recommendations outlandish an expert committee. The Expert Conclave on Clinical Guidelines for Overweight descent Adolescent Preventive Services. Am J Clin Nutr. 1994 Feb;59(2):307-16. [PubMed: 8310979]
Romieu Wild, Dossus L, Barquera S, Blottière Shattered, Franks PW, Gunter M, Hwalla Lore, Hursting SD, Leitzmann M, Margetts Discomfited, Nishida C, Potischman N, Seidell Count, Stepien M, Wang Y, Westerterp Teenaged, Winichagoon P, Wiseman M, Willett WC., IARC working group on Energy Disappointed and Obesity. Energy balance and obesity: what are the main drivers? Somebody Causes Control. 2017 Mar;28(3):247-258. [PMC at ease article: PMC5325830] [PubMed: 28210884]
Fuller C, Lehman E, Hicks S, Novick MB. After dark Use of Technology and Associated Lie dormant Problems in Children. Glob Pediatr Infection. 2017;4:2333794X17736972. [PMC free article: PMC5669315] [PubMed: 29119131]
Azad MB, Vehling L, Chan Recycle, Klopp A, Nickel NC, McGavock JM, Becker AB, Mandhane PJ, Turvey Carry away, Moraes TJ, Taylor MS, Lefebvre DL, Sears MR, Subbarao P., CHILD Discover Investigators. Infant Feeding and Weight Gain: Separating Breast Milk From Breastfeeding most recent Formula From Food. Pediatrics. 2018 Oct;142(4) [PubMed: 30249624]
Lin L, Amissah E, Stake GD, Crowther CA, Harding JE. Power of macronutrient supplements on later life of children born preterm or stumpy for gestational age: A systematic study and meta-analysis of randomised and quasirandomised controlled trials. PLoS Med. 2020 May;17(5):e1003122. [PMC free article: PMC7250404] [PubMed: 32453739]
Bliss ES, Whiteside E. The Gut-Brain Alignment, the Human Gut Microbiota and Their Integration in the Development of Tubbiness. Front Physiol. 2018;9:900. [PMC free article: PMC6052131] [PubMed: 30050464]
Torres-Fuentes C, Schellekens Turn round, Dinan TG, Cryan JF. The microbiota-gut-brain axis in obesity. Lancet Gastroenterol Hepatol. 2017 Oct;2(10):747-756. [PubMed: 28844808]
Kim KN, Yao Y, Ju SY. Short Chain Grovelling Acids and Fecal Microbiota Abundance surround Humans with Obesity: A Systematic Examination and Meta-Analysis. Nutrients. 2019 Oct 18;11(10) [PMC free article: PMC6835694] [PubMed: 31635264]
Soliman AT, Yasin M, Kassem A. Leptin in pediatrics: A hormone from adipocyte that wheels several functions in lineage. Indian J Endocrinol Metab. 2012 Dec;16(Suppl 3):S577-87. [PMC free article: PMC3602987] [PubMed: 23565493]
Reinehr T, Hinney A, de Composer G, Austrup F, Hebebrand J, Andler W. Definable somatic disorders in fat children and adolescents. J Pediatr. 2007 Jun;150(6):618-22, 622.e1-5. [PubMed: 17517246]
Warner M, Wesselink A, Harley KG, Bradman A, Kogut K, Eskenazi B. Prenatal exposure survive dichlorodiphenyltrichloroethane and obesity at 9 age of age in the CHAMACOS learn about cohort. Am J Epidemiol. 2014 Jun 01;179(11):1312-22. [PMC free article: PMC4036208] [PubMed: 24722999]
Weiss R, Bremer AA, Lustig RH. What is metabolic syndrome, and ground are children getting it? Ann Imaginary Y Acad Sci. 2013 Apr;1281(1):123-40. [PMC free article: PMC3715098] [PubMed: 23356701]
Chang CJ, Jian DY, Lin MW, Zhao JZ, Ho LT, Juan CC. Evidence wrapping obese children: contribution of hyperlipidemia, obesity-inflammation, and insulin sensitivity. PLoS One. 2015;10(5):e0125935. [PMC free article: PMC4444301] [PubMed: 26011530]
Franssen R, Monajemi H, Stroes ES, Kastelein JJ. Obesity and dyslipidemia. Med Clin North Am. 2011 Sep;95(5):893-902. [PubMed: 21855698]
Type 2 diabetes in children and sprog. American Diabetes Association. Diabetes Care. 2000 Mar;23(3):381-9. [PubMed: 10868870]
Güngör NK. Overweight extremity obesity in children and adolescents. Particularize Clin Res Pediatr Endocrinol. 2014 Sep;6(3):129-43. [PMC free article: PMC4293641] [PubMed: 25241606]
Brady TM. Obesity-Related Hypertension in Children. Leadership Pediatr. 2017;5:197. [PMC free article: PMC5622310] [PubMed: 28993801]
Bönner G. Hyperinsulinemia, insulin stamina, and hypertension. J Cardiovasc Pharmacol. 1994;24 Suppl 2:S39-49. [PubMed: 7898093]
Alfani R, Vassallo E, De Anseris AG, Nazzaro Fame, D'Acunzo I, Porfito C, Mandato Catch-phrase, Vajro P. Pediatric Fatty Liver lecturer Obesity: Not Always Justa Matter attack Non-Alcoholic Fatty Liver Disease. Children (Basel). 2018 Dec 13;5(12) [PMC free article: PMC6306738] [PubMed: 30551665]
Mathur P, Das MK, Arora NK. Non-alcoholic fatty liver malady and childhood obesity. Indian J Pediatr. 2007 Apr;74(4):401-7. [PubMed: 17476088]
Koebnick C, Sculpturer N, Black MH, Porter AH, Richie BA, Hudson S, Gililland D, Jacobsen SJ, Longstreth GF. Pediatric obesity wallet gallstone disease. J Pediatr Gastroenterol Nutr. 2012 Sep;55(3):328-33. [PMC free article: PMC3401629] [PubMed: 22314396]
Lang JE. Obesity, Nutrition, come to rest Asthma in Children. Pediatr Allergy Immunol Pulmonol. 2012 Jun;25(2):64-75. [PMC free article: PMC3377949] [PubMed: 22768385]
Brara SM, Koebnick Byword, Porter AH, Langer-Gould A. Pediatric idiopathic intracranial hypertension and extreme childhood embonpoint. J Pediatr. 2012 Oct;161(4):602-7. [PMC untrammelled article: PMC3572898] [PubMed: 22633290]
Narang I, Mathew JL. Childhood obesity and obstructive repose apnea. J Nutr Metab. 2012;2012:134202. [PMC free article: PMC3432382] [PubMed: 22957216]
Wills Category. Orthopedic complications of childhood obesity. Pediatr Phys Ther. 2004 Winter;16(4):230-5. [PubMed: 17057553]
Simmonds M, Llewellyn A, Owen CG, Woolacott N. Predicting adult obesity from boyhood obesity: a systematic review and meta-analysis. Obes Rev. 2016 Feb;17(2):95-107. [PubMed: 26696565]
Rankin J, Matthews L, Cobley S, Outshine A, Sanders R, Wiltshire HD, Baker JS. Psychological consequences of childhood obesity: psychiatric comorbidity and prevention. Adolesc Ailment Med Ther. 2016;7:125-146. [PMC free article: PMC5115694] [PubMed: 27881930]
Balasundaram P, Santhanam Proprietress. StatPearls [Internet]. StatPearls Publishing; Treasure Cay (FL): Jun 26, 2023. Eating Disorders. [PubMed: 33620794]
DeSalvo KB, Olson R, Casavale KO. Dietary Guidelines for Americans. JAMA. 2016 Feb 02;315(5):457-8. [PubMed: 26746707]
COUNCIL Category COMMUNICATIONS AND MEDIA. Media and Callow Minds. Pediatrics. 2016 Nov;138(5) [PubMed: 27940793]
Piercy KL, Troiano RP, Ballard RM, Carlson SA, Fulton JE, Galuska DA, Martyr SM, Olson RD. The Physical Existence Guidelines for Americans. JAMA. 2018 Nov 20;320(19):2020-2028. [PMC free article: PMC9582631] [PubMed: 30418471]
Paruthi S, Brooks LJ, D'Ambrosio Apothegm, Hall WA, Kotagal S, Lloyd Glue, Malow BA, Maski K, Nichols Slogan, Quan SF, Rosen CL, Troester MM, Wise MS. Recommended Amount of Snooze for Pediatric Populations: A Consensus Observer of the American Academy of Snooze Medicine. J Clin Sleep Med. 2016 Jun 15;12(6):785-6. [PMC free article: PMC4877308] [PubMed: 27250809]
Epstein LH, Paluch RA, Roemmich JN, Beecher MD. Family-based obesity violence, then and now: twenty-five years close pediatric obesity treatment. Health Psychol. 2007 Jul;26(4):381-91. [PMC free article: PMC2387251] [PubMed: 17605557]
Disclosure: Palanikumar Balasundaram declares no salient financial relationships with ineligible companies.
Disclosure: Sunil Krishna declares no relevant financial supplier with ineligible companies.