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Obesity and over weight are terms that are commonly used interchangeably. In children with overweight being the preferred one. The incidence of childhood obesity has increased rapidly in the last decade. This is impacting not only the developed countries but also affecting the developing world. Childhood obesity has serious short and long term medical consequences.


Criteria for Obesity


Obesity implies excessive fat and not merely excess weight. Body weight is thus not reliable criterion for defining obesity. As methods of measuring body fat are cumbersome and expensive, several clinical and anthropo­metric parameters are used as markers of obesity.


Body mass index: Body mass index (BMI) is the most widely used parameter to define obesity. It takes into account weight as well as the height. It is calculated by the formula:

BMI = Weight (kg) height (m)2

Children with BMI more than 85 percentile for age are considered at-risk for obesity while those more than 95 percentile for age are obese. BMI is a good indicator of body fat but is unreliable in short muscular individuals.


WHO defines :


Overweight : BMI 25


Obesity : BMI 30


Weight for height: This compares the child's weight to the expected weight for his/her height. Weight for height more than 120% is diagnosed as obesity.


Skill fold thickness: Skin fold thickness measured over the subscapular, triceps or biceps regions is an indicator for subcutaneous fat. Age specific percentile cut-offs should be used with values more than 85 percentile being abnormal.


Waist circumference: This is a marker of abdominal adiposity, a key risk factor for metabolic and cardio­vascular effects of obesity.



In most children with obesity, environmental and hereditary factors play the major role. Underlying etiology is identified in very few cases (less than 1%).

Constitutional obesity: Most children with obesity do not have an organic cause. This is caused by imbalance in energy intake and expenditure. These children are tall for age, a factor that differentiates them from pathological obesity. They have proportional obesity and normal development. Important environmental influences include excessive calorie intake, sedentary lifestyle, television viewing and playing computer games. It is important to identify this subgroup of children to avoid unnecessary investigations.


Endocrine causes: Though rare, identification of endocrine etiology of obesity has important management impli­cations. Growth failure in an obese child is an important marker of an underlying endocrine cause. Cushing syndrome is characterized by central obesi ty, hypertension, striae and retarded skeletal maturation. Hypothyroidism is an extremely rare cause of isolated obesity and other features like developmental delay and coarse skin are always present. In GH deficiency and pseudohypopara­thyroidism, growth retardation and hypocalcemia are dominant clinical features and obesity is a less prominent manifestation. Endocrine cause of obesity is unlikely in a child with normal growth.


Genetic syndromes: A variety of genetic syndromes have obesity as their major clinical feature. Many of these syndromes are associated with hypogonadism or hypotonia (Prader Willi, Carpenter and Laurence Moon Biedl Bardet syndromes).


Table: Etiology of obesity




Environmental factors (over 95% of all cases)


  1. Endocrine: Cushing syndrome, GH deficiency, hypo­thyroidism, pseudohypoparathyroidism
  2. Hypothalamic: Head injury, infection, brain tumor, radiation, post-neurosurgery
  3. Drugs: Antiepileptic drugs, steroids, estrogen
  4. Genetic syndromes: Prader Willi, Laurence Moon Biedl Bardet, Beckwith Weidemann, Carpenter syndromes
  5. Monogenic disorders: Leptin deficiency, leptin resistance, abnormalities of MC4 receptor and proconvertase  

Hypothalamic obesity: CNS insults due to surgery, radiation, tumors and trauma results in rapid onset obesity. These disorders are associated with excessive appetite, signs and symptoms of CNS involvement and other hypothalamic pituitary defects.


Monogenic obesity: Monogenic obesity represents a very small proportion of children with obesity. They are more likely in the presence of early onset of obesity, morbid obesity and strong family history. Leptin deficiency was the first monogenic cause of obesity identified. Inefficient leptin action (deficiency or resistance) results in uncon­trolled appetite and obesity. Abnormalities in mineralo­corticoid receptor and proconvertase have also been associated with obesity.




Initial evaluation is guided to differentiate constitutional from pathological obesity (Table 16.24). Normal growth, generalized pattern and lack of developmental delay or dysmorphism suggests constitutional obesity and against the need for extensive investigations.


Comparison of constitutional and pathological obesity

Feature obesity

Constitutional obesity




Bone age






Usually central



May be present


Clinical: Family history of obesity and its complications should be recorded. Detailed history of physical activity, dietary recall and periods of inactivity shou ld be assessed. Increased appetite in a child with recent onset obesity may indicate the possibility of a hypothalamic lesion. Delayed develop men t points towards genetic syndromes associa ted with obesity. Features of raised intracranial tension along with history of CNS infection, head trauma or neuro­surgery should point towards the diagnosis of CNS cause of obesity. Intake of drugs linked with development of obesity like steroids and antiepileptics should be inquired. Features of daytime somnolence or sleep apnea are suggestive of obesity severe enough to produce respiratory embarrassment. Examination for features of endocrino­pathies, dysmorphic syndromes and complications such as hypertension and acanthosis nigricans should be perfor­med. Special emphasis should be given to sexual maturity and ocular examination. Hypogonadism is an important feature of obese children with Laurence Moon Biedl syndrome and Prader Willi syndromes.


Features of pathological obesity



Prader Willi syndrome

Infantile hypotonia, hyperphagia, almond like eyes, acromicria, hypogonadism, behavioral abnormality

Laurence Moon Biedl Bardet syndrome


Hypogonadism, retinitis pigmentosa, polydactyly, renal abnormalities, mental retard a tion

Beckwith Wiedemann syndrome

Organomegaly, ear lobe creases, hemihypertrophy

Cushing syndrome


Hirsutism, central obesity, growth retardation, striae, buffalo hump, hypertension, myopathy


Growth retardation, coarse facies, developmental delay


Tetany, osteodystrophy


Increased growth rate, normal facies, family history


Investigations: Investigations are decided based on the degree of obesity and associated complications. Endocrine investigations are done only in the presence of pointers to diagnosis such as growth failure, clinical features, developmental delay, and dysmorphism. Screening for complications is indicated in obese children (BMI more than 95th percentile). Investigations are also recom­mended for overweight children in the presence of family history of cardiovascular complications or type 2 DM or rapid increase in obesity. This evaluation should include oral glucose tolerance test, serum cholesterol and liver function tests.




Childhood obesity is associated with significant complications.


Table 16.27: Complications of obesity Complication




Central nervous system













Benign intracranial hypertension


Obstructive sleep apnea


Atherosclerosis, hypertension


Nonalcoholic steatohepatitis (NASH),Q  gall stone disease


Polycystic ovarian disease, type 2 diabetes mellitus, dyslipidemia


Slipped capital femoral epiphyses, Blount's disease, osteoarthritis


Cardiovascular: Obesity has been linked with hyper­lipidemia, hypertension and coronary artery disease. This is associated with significant risk of adverse cardio­vascular effects in early adulthood. Metabolic syndrome, a combination of insulin resistance, hypertension and hyperlipidemia, is in particular an important complication of obesity.

: Most important endocrine complication of obesity is insulin resistance. This presents as a spectrum of changes ranging from elevated insulin levels to impaired glucose tolerance to type 2 DM. A characteristic clinical feature is acanthosis nigricans, dark and rough areas on the exposed areas of skin including back of neck, axilla and thigh. Ovarian hyperandrogenism leading to premature adrenarche and polycystic ovarian syn­drome is an important feature of obesity.


Respiratory: Obesity is associated with restrictive (decreased respiratory movements due to obesity) as well as obstructive pulmonary disease (fat deposition in the airway). The most severe respiratory complication is the obesity-hypoventilation syndrome associated with hypoxia and features of cor pulmonale. In its milder form, it is associated with snoring, irritability, hyperactivity and daytime somnolence.


Orthopedic: Obese children are prone to slipped femoral epiphyses, flat feet, Blount's disease (tibia vara) and early onset osteoarthritis.


Hepatobiliary: Insulin resistance in obesity is associated with fatty infiltration in liver. This may vary from mild infiltration with no effect to steatohepatitis to chronic liver disease. The incidence of cholelithiasis is greater in obese children and has been shown to increase with treatment for obesity.



Management of childhood obesity is challenging with major impetus on lifestyle measures (Fig 16.16). Specific management is available for only a few conditions. Diet, activity and behavioral measures are the cornerstones of therapy with intensive measures like drug therapy and surgery reserved for morbid cases.


Dietary measures: Initial dietary measure includes mild caloric restriction and alteration in dietary habits. Intake of 1200-1800 calories depending upon the age of the individual with 30--40% restriction is recommended. Over­aggressive dietary restriction is associated with poor compliance and growth faltering. Apart from restricting calorie intake, efforts should be directed towards improving the nutritive value of the diet. Reduction in consumption of junk foods, carbonated drinks and saturated fat along with an increase in fiber, fruits and vegetable intake are helpful in improving body composi­tion. Regular meal consumption with fixed portion size is an effective strategy in inducing weight gain.

Lifestyle modification:
Increase in physical activity along with reduction in sedentary lifestyle is an important part of obesity management. Swimming, running and playing outdoor games should be encouraged. Physical activity for at least 30-45 minutes per day should be recom­mended. Activities like television viewing, videogames and internet surfing should be restricted.


Drugs: Drug therapy is reserved only for severe cases of obesity. There is limited data regarding the use of anti­obesity drugs in children. The only drugs that have been tried in adolescents include orlistat (gastric lipase inhibitor) and sibutramine (neurotransmitter modulator). Metformin is indicated in children with insulin resistance. It has the added advantage of inducing weight loss. Leptin (for those with leptin deficiency) and octreotide (for hypothalamic obesity) are promising approaches for subgroups of child­ren with obesity. The efficacy of pharmacological therapy for obesity has however been modest compared to surgery.


Surgery: Surgery for obesity is the last resort in treatment. It is indicated for morbid obesity (BMI more than 40 kg/m2 with complications) after they have filled 6 months of multidisciplinary weight management programme.   

Laparoscopic gastric banding is the procedure of choice and is directed at reducing gastric capacity. Q This results in reduced appetite and weight loss. Experience with obesity surgery in children is limited but has been shown to cause significant reduction in body weight sustained for a period of 1 year.


Initial management should be directed towards lifestyle modification with increased physical activity and nutritional advice. Metformin should be considered if clinical or laboratory features of insulin resistance are present. Children with morbid obesity with no response to lifestyle measures are candidates for surgery and medications.


Overweight: Weight exceeds 110 percent or skin-fold thickness is more than 30 mm.



  1. Weight exceeds 120 percent.
  2. The body mass index (BM1) defined, as weight/height (in kg/m2) is the most useful index ('or screening population of young children and adolescents.
  3. Skin-fold thickness above 85 percentile for age and sex also suggest obesity.

Endogenous Obesity


Genetic causes


Prader-Willi syndrome - Severe hypotonia and areflexia causing feeding difficulty at birth.


Between the ages 6 months to 2 years the child shows hyperphagia leading to obesity.

  1. Pickwickian syndrome
  2. Short stature
  3. Hypogonadotropic hypogonadism
  4. 2/3rd  of patients show deletion on short arm of chromosome 15

Lawrence Moon-Biedl Bardet Syndrome

Mild to moderate MR, obesity, polydactyly or syndactyly Q, retinitis pigmentosa, renal anomalies and hypogonadism.


Hypothalamic Obesity

Frohlich syndrome
Q - is characterized by obesity, short stature, hyperphagia (due to increased appetite). sexual infantilism and sometimes blindness.

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