In childhood, obesity may be assessed in different ways. Measurement of weight alone is inadequate, given the influence of height on weight. Although obesity may be clinically obvious if the child’s weight centile is greater than the height centile, the severity of obesity is better defined by the use of the body mass index (BMI) in which


It should be noted that although excess BMI is good at identifying excess weight, it does not distinguish between fat and lean tissue and in unusual circumstances (e.g. heavy‐weight sports) may not indicate excess fat. Alternatively, body fatness can be assessed from direct measurements of subcutaneous skinfold thickness using skinfold thickness callipers or from measurement of waist circumference. Given the normal variations of BMI, skinfold thickness and waist circumference through childhood, reference to centile charts is required for interpretation of the data. The utility of skinfold thickness and waist circumference measurements is limited by the practical difficulties of obtaining these measurements accurately and so measurement of BMI is currently the best clinical method for identifying and monitoring obesity in childhood.

There are no universally agreed definitions of obesity in childhood as there are few data correlating specific definitions with future health risks. In practice in the United Kingdom, children with a BMI above the age‐ and sex‐specific 91st centile can be defined as overweight and those above the 98th centile as clinically obese (see Appendix 1 for sex‐specific BMI centile reference charts). Throughout the industrialized world, there is clear evidence of a rapid increase in the prevalence of obesity in children and adults, with older children more affected than infants and those from Hispanic and non‐Hispanic black communities in the United States more affected than non‐Hispanic whites. In the United States, more than 20% of 12–19‐year‐old children have a BMI that exceeds the 95th centile (the US definition of obesity).


An increased risk of obesity is associated with genetic, environmental (Table 11.1), and pathological factors (Table 11.2). It is likely that a combination of an increasingly sedentary lifestyle combined with an excessive calorie intake for need is principally responsible for the rapid increase in the prevalence of obesity noted in recent decades.

Table 11.1 Non‐pathological risk factors for obesity.

Risk factor Examples
Genetic Obesity in either or both parents

Early adiposity rebound
Environmental Socio‐economic deprivation

Single child

Single parent
Diet‐related Bottle‐fed in infancy

High fat diet

Disorganized eating patterns
Activity‐related Physical inactivity

Increased television watching

Short sleep duration

Table 11.2 Pathological causes of excess body weight.

Cause Examples
Syndromes Laurence–Moon–Biedl syndrome

Down’s syndrome

Prader–Willi syndrome (Figure 11.2)
Single gene mutations Melanocortin‐4 receptor



Leptin receptor

GNAS (pseudohypoparathyroidism)
Hypothalamic damage Trauma

Tumours, e.g. craniopharyngioma

Post encephalitis
Endocrine abnormalities Growth hormone deficiency


Cushing’s syndrome

Immobility Spina bifida

Cerebral palsy
Impaired skeletal growth Achondroplasia
Drugs Insulin


Antithyroid drugs

Sodium valproate

Antipsychotics e.g. risperidone

Obese children under three years of age without obese parents are at low risk of obesity in adulthood. However, in older children, the presence of obesity becomes an increasingly important predictor of adult obesity, regardless of whether the parents are obese or not, with more than two‐thirds of children who are obese aged 10 years or older becoming obese adults. Parental obesity more than doubles the risk of adult obesity in young children. Twin studies have suggested a heritability of fat mass of 40–70%.

Regulation of body fat

The normal amounts of body fat change through childhood, as can be seen from the BMI centile charts (see Appendix 1). Infants gain fat, as a consequence of increasing adipose cell size, relatively rapidly until the age of one year, but then slim down until the age of approximately six years as adipose cells reduce in size. From this point onwards, there is a steady increase in body fat into young adult life (the so‐called ‘adiposity rebound’) associated with increases in adipose cell numbers. There is little difference in the amount of body fat in infant girls and boys. However, after infancy, subcutaneous fat increases more rapidly in girls, particularly during puberty when males demonstrate greater centralization of body fat stores.

Obesity occurs when energy intake chronically exceeds energy expenditure. In obese children there are wide variations in energy intake and not all obese children eat excessively. The high calorie density and fat content of the modern diet are associated with an increased risk of obesity.

The hypothalamus has a central role in the regulation of energy balance, integrating neuronal, hormonal, and nutrient messages from within the body and transmitting signals which lead to the sensations of hunger or satiety (Figure 11.1). The hypothalamus also influences energy expenditure via autonomic nerve function and the regulation of pituitary hormone release. Many hypothalamic neurotransmitters have been shown to influence energy intake (Table 11.3).

Diagram of a brain illustrating the influences on the hypothalamic control of satiety, with lines marking circulating nutrients, gastrointestinal tract, etc. and pointed by an arrow labeled taste, memory, behavioural factors. Downward arrows are also labeled central nervous system, autonomic nervous system, and pituitary hormones.

Figure 11.1 Influences on the hypothalamic control of satiety.

Table 11.3 Factors which influence the central nervous system regulation of energy intake.

Factors which increase food intake Factors which decrease food intake
Noradrenaline Serotonin
Opioids (e.g. dynorphin and β‐endorphin) Dopamine
Ghrelin Cholecystokinin
Galanin Corticotrophin‐releasing factor
Neuropeptide Y Neurotensin
Melanin‐concentrating hormone Bombesin
Agouti‐related peptide Calcitonin gene‐related peptide
Orexins A and B (hypocretins 1 and 2) Thyrotropin‐releasing hormone
Growth hormone‐releasing hormone Amylin


Peptide YY3−36



Glucagon‐like peptide 1

α‐Melanocyte stimulating hormone

Cocaine‐ and amphetamine‐related peptide


Energy expenditure consists of the following three components:

  1. Resting metabolic rate is the energy expended at rest for the maintenance of basic cellular activities, excluding maintenance of body temperature, and it accounts for 60–70% of total energy expenditure. Fat‐free mass is metabolically more active than fat mass. Obese individuals have increased amounts of both body fat and fat‐free mass and therefore most obese individuals have increases in their absolute resting metabolic rates because of their increased fat‐free mass.
  2. Thermogenesis is the energy expended in response to digestion and absorption of food, temperature changes, emotional influences or drugs which influence the physiological responses to such stimuli. It accounts for about 10% of total energy expenditure. It is unlikely that variations in thermogenesis are clinically important in the energy balance of the obese individual.
  3. Energy expended in physical activity in children varies widely both on an individual daily basis and between individuals and accounts for 20–30% of total energy expenditure. Although obese children may be relatively physically inactive, they have an increase in the energy cost of weight‐bearing activities and therefore do not demonstrate marked reductions in this component of energy expenditure when compared to normal‐weight children.

As a consequence of these influences on energy expenditure, in most obese children, absolute total energy expenditure is increased. However, there is evidence that a low relative metabolic rate (i.e. adjusted for body size) predisposes to weight gain.

Complex interactions exist between signalling pathways that control energy intake and satiety and those that regulate fat mass. Adipose tissue may influence the hypothalamic regulation of the energy balance through the secretion of leptin, a hormone which crosses the blood–brain barrier and suppresses the production of neuropeptide Y within the hypothalamus, leading to reduced appetite and increased energy expenditure. However, most obese children have increased leptin concentrations in proportion to their increased body fat mass. Disorders of leptin synthesis or action (leptin receptor mutations) are very rare and account for few cases of obesity.

Preliminary examination and investigation


Most children with obesity do not have an underlying pathological cause and have so‐called ‘simple obesity’, also known as exogenous obesity. Such children usually demonstrate rapid growth and physical development. By contrast, children who are obese, short, and growing slowly are much more likely to have an endocrine abnormality or, if associated with dysmorphic features and intellectual impairment, a syndromic cause to their obesity. A careful history and examination are required to distinguish the few children with significant underlying pathology causing their obesity from those who have ‘simple obesity’. The history should include the following details:

  • Birth weight: if increased, this suggests an underlying mechanism, such as hyperinsulinism, which may have started in utero.
  • Age of onset of obesity: early onset of obesity (before the age of two years) or while exclusively breast‐fed is more suggestive of a genetic or syndromic cause.
  • Presence of congenital abnormalities or symptoms suggestive of a syndrome: e.g. initial feeding problems requiring nasogastric tube feeds and hypotonia with certain dysmorphic features might suggest Prader–Willi syndrome (Figure 11.2).
  • Detailed feeding and dietary history: it is often useful to go through a typical day’s diet. Ravenous appetite and lack of satiety suggest a rare genetic cause of obesity.
  • Information about levels of physical activity.
  • The extent to which the obesity may be having adverse effects on the child: if these are particularly psychosocial or related to school. Also the extent of the desire of the child and parents for the child to lose weight and the extent and success of previous interventions to achieve weight control.
  • Medication.
  • Symptoms of hypothalamo–pituitary pathology: e.g. headache, visual symptoms or previous history of trauma or encephalitis.
  • Symptoms suggestive of endocrine abnormality (Table 11.2).
  • Presence of polydipsia and polyuria: these are indicative of type 2 diabetes.
  • Family history of obesity.
Photo of a boy with Prader–Willi syndrome.

Figure 11.2 Prader–Willi syndrome.

Source: M. Donaldson, Glasgow.


On examination, the child should undergo an accurate assessment of height and weight with measurements plotted on height, weight, and BMI centile charts. Height measurements should be compared with the target height range derived from the mid‐parental height centile, as those who are relatively short for their genetic background are more likely to have a syndromic or endocrine cause for their obesity, whereas those who are relatively tall are more likely to suffer from simple obesity. Further assessment of the severity of the obesity can be made from the measurement of waist circumference or triceps and subscapular skinfold thickness, although these measurement techniques require training and are difficult to perform in very obese individuals. Not all pathological causes of obesity will be self‐evident and careful clinical examination is required to identify signs suggestive of certain disorders or complications of obesity. It is particularly important to note the presence of acanthosis nigricans most commonly seen in the axillae or neck (see Figure 1.9), as this may indicate evolving insulin resistance and an increased risk of developing type 2 diabetes. Key signs to note on clinical examination are shown in Table 11.4. The clinical features of syndromes, which may present with obesity, are summarized in Table 11.5.

Table 11.4 Clinical signs to look for on examination.

Clinical sign Possible diagnosis
Acanthosis nigricans Type 2 diabetes (insulin resistance)
Hypertension Syndrome X (metabolic syndrome)
Dysmorphic features (see Table 11.5) Laurence–Moon–Biedl syndrome (Figure 11.3)

Prader–Willi syndrome (Figure 11.2)

Pseudohypoparathyroidism (Figure 11.4)

Beckwith–Wiedemann syndrome
Impaired visual fields Intracranial tumour, e.g. craniopharyngioma
Papilloedema or optic atrophy
Tall stature or increased height velocity Simple obesity, hyperinsulinism
Short stature or decreased height velocity Growth hormone deficiency, hypothyroidism, Laurence–Moon–Biedl syndrome

Prader–Willi syndrome

Cranial midline defects (e.g. cleft lip and palate) Growth hormone deficiency
Truncal obesity
Goitre Hypothyroidism
Prolonged ankle tendon reflexes
Proximal myopathy Cushing’s syndrome
Truncal obesity
Abnormal gait Spina bifida

Cerebral palsy
Image described by caption.

Figure 11.3 Polydactyly in a child with Laurence–Moon–Biedl syndrome.

Image described by caption.

Figure 11.4 Shortening of the fourth metacarpal (a) and metatarsal (b) in pseudohypoparathyroidism.

Table 11.5 Clinical features of common syndromic causes of obesity (Figures 11.211.4).

System Prader–Willi syndrome Laurence–Moon–Biedl syndrome Pseudohypo‐parathyroidism
Facial Narrow forehead Squint Round facies

Olive‐shaped eyes
Short neck

Antimongoloid slant

Epicanthic folds


Carp mouth


Abnormal ear lobes
Skeletal Short stature Short stature Short stature

Small hands and feet Polydactyly Shortened fourth metacarpals and metatarsals

Clinodactyly Clinodactyly



Dislocated hips
Neurosensory development and behaviour ↓ IQ ↓ IQ ↓ IQ

Hypotonia and feeding problems in infancy Retinitis pigmentosa

Insatiable appetite

Uncontrollable rage
Endocrine Hypogonadotrophic hypogonadism Hypogonadotrophic hypogonadism PTH‐resistant hypocalcaemia

Type 2 diabetes Diabetes insipidus
Renal anomalies Subcutaneous calcifications


The main adverse effects of obesity are summarized in Table 11.6. In childhood, acute medical complications of simple obesity are usually few and minor. The combination of insulin resistance, hypertension, hypertriglyceridaemia, and a low concentration of high‐density lipoprotein (HDL) cholesterol (so‐called ‘metabolic syndrome’) used to be rarely seen in childhood, although in the United States, nowadays, one in four overweight children in the age group 6–12 years has impaired glucose tolerance and 60% of these have at least one risk factor for heart disease. There are particular concerns about the increased prevalence of obesity and its metabolic complications in ethnic minority groups in both Europe and North America. Furthermore, being overweight in childhood has been shown to be a major risk factor for the development of the metabolic syndrome and coronary artery disease in adult life. Long‐standing obesity leads to children being tall for their age, relative to genetic height potential, and to an advanced bone age (so that adult height is not increased). Why excess body fat has this effect is unclear. Obese children may also have an impaired self‐image and for boys this may be complicated by a marked suprapubic fat pad leading to the penis being buried in fat and, as a result, appearing very small.

Table 11.6 Complications of simple obesity.

System Adverse effect
Metabolic and endocrine Hyperinsulinaemia

Impaired glucose tolerance

Type 2 diabetes


Metabolic syndrome

Advanced pubertal development

Polycystic ovarian disease

Non‐alcoholic steatohepatitis (NASH)

Cardiovascular Hypertension
Respiratory Breathless on exertion

Obstructive sleep apnoea

Pickwickian syndrome
Skeletal Knock knee or bow legs

Slipped capital femoral epiphysis
Skin Furunculosis

Neurological Idiopathic intracranial hypertension
Psychological Poor self‐image


Behavioural problems




The following investigations should be considered in those in whom there is clinical concern regarding an underlying pathological cause or a possible metabolic complication of obesity:

  • An assessment of glucose tolerance, fasting blood glucose or, occasionally, an oral glucose tolerance test.
  • Increased fasting serum insulin and decreased sex‐hormone‐binding globulin concentrations may confirm the presence of insulin resistance.
  • Lipid profile.
  • Thyroid function tests (TFTs) (serum thyroxine [T4] and thyroid‐stimulating hormone [TSH] concentrations). However, in the absence of clinical evidence of hypothyroidism such as decreased linear growth, TSH should NOT be measured. Indeed, the mild hyperthyrotropinemia often seen in exogenous obesity is not causally related to it and disappears if weight loss is achieved.
  • Liver function tests.
  • Three 24‐hour urinary cortisol estimations.
  • Bone age.
  • Serum luteinizing hormone (LH), follicle‐stimulating hormone (FSH), oestradiol, 17‐hydroxy progesterone, androstenedione, and testosterone concentrations and a pelvic ultrasound in a girl with hirsutism or menstrual irregularity thought to be at risk of having polycystic ovarian syndrome. The need for additional investigations will depend on the level of clinical concern.
  • In cases of suspected or proven hypothyroidism, Cushing’s syndrome, hyperinsulinism or growth hormone (GH) deficiency, consult the relevant chapters in this volume for further investigations.
  • If Laurence–Moon–Biedl syndrome is suspected, referral to a geneticist may be of help in identifying the relevant dysmorphic features and referral to an ophthalmologist for detailed retinal examination, including electroretinography, is important. Renal function should be assessed.
  • Prader–Willi syndrome can be confirmed molecularly by methylation studies of chromosome 15q11‐13.
  • If pseudohypoparathyroidism is suspected, measure serum calcium, phosphate and parathyroid hormone (PTH) concentrations. In the case of a low serum calcium and elevated phosphate and PTH, the diagnosis may be confirmed by demonstration of inactivating mutations of the GNAS gene which encodes the G protein stimulatory, alpha subunit which is located on the long arm of chromosome 20.
  • In syndromes associated with hypogonadism, investigation of the pituitary–gonadal axis should be considered in those who have genital hypoplasia, markedly delayed puberty or inadequate development of secondary sex characteristics (see Chapter 5).


Young infants frequently appear fat and a spontaneous reduction in body fat occurs as part of the normal changes in body composition with increasing age. In general, therefore, it is rare that a slimming regimen needs to be considered in the young child. However, investigations to exclude a pathological cause of obesity should be undertaken in all infants with severe, early onset obesity. If calorie restriction is deemed necessary in infancy, the aim should be maintenance of body weight rather than weight loss, as the latter may lead to specific dietary (e.g. vitamin) deficiencies or growth failure.

For many obese children, weight loss down to an ‘ideal body weight for height’ is probably unrealistic. Nevertheless, more modest weight reduction, or even prevention of further weight gain, may produce significant long‐term health benefits. Such goals, which are more likely to be achievable, should be considered when planning individual therapeutic regimens. Unfortunately, there is almost no published evidence for any effective treatment for childhood obesity.

Older children with simple obesity should be encouraged to try and control their weight gain by:

  • educating about the nature of obesity and its long‐term consequences;
  • realistic assessment of the ease and likely benefits of slimming regimens;
  • healthy eating (e.g. regular family meal times, avoidance of excessive ‘snacking’, fried foods, added fats and sugars, and high energy drinks, while encouraging foods with high fibre content) with modest calorie restriction and advice from a dietician where necessary;
  • increasing habitual physical activity (e.g. walking rather than taking transport to school, participation in games or sports that the child enjoys, restricting television or computer games);
  • psychological support (e.g. regular attendance at a dedicated clinic with dietetic support, group therapy, such as Weight Watchers, with the emphasis on mutual support, promotion of positive self‐esteem and enhancing motivation to change life‐style factors).

Once a child has developed significant obesity, both weight loss and long‐term maintenance of an improved body weight become difficult to achieve. Encouragement for children with simple obesity is best provided by frequent visits (e.g. three‐monthly) by the patient to a clinic or support service with motivated and interested staff. Multidisciplinary services involving community paediatricians, general practitioners, dieticians, psychologists, or psychiatrists may help to improve the outcome. However, there is no point in continuing to encourage attendance in obese patients who do not adhere to suggested interventions and who do not achieve significant weight loss, although intermittent clinical follow‐up to monitor for early signs of the complications of obesity may still be necessary.

Although medical therapy, including inhibitors of nutrient absorption from the gut (e.g. acarbose, guar gum, and pancreatic lipase inhibitors), appetite suppressants (e.g. amphetamine derivatives and serotoninergic agents) and agents which increase energy expenditure (e.g. T4 and adrenergic agonists), have been used in the treatment of obesity in adults, there is little experience of their use and efficacy in childhood. Side effects may be problematic and their use is not currently recommended in children. There has also been recent interest in the potential benefits of metformin though results of randomized trials have proved disappointing and treatment of obesity in the absence of type 2 diabetes with metformin is not routinely advised.

There is increasing interest in the value of bariatric surgical interventions, such as laparoscopic gastric banding or the Roux‐en‐Y gastric bypass procedure in extremely obese children. When undertaken in children, dramatic amounts of weight loss can be achieved although such children will require careful monitoring for side effects in specialist clinical services.

Where excessive weight is the consequence of an underlying endocrinopathy, treatment of hormone deficiency with the relevant hormone replacement (e.g. GH or T4) should result in a decrease in body fat. There is evidence that Prader–Willi syndrome is associated with hypothalamic dysfunction, including impaired GH secretion. GH therapy (0.25 mg/kg per week to a maximum of 2.7 mg daily) is now widely used for the improvement of growth and body composition in children with Prader–Willi syndrome, providing there is no evidence of upper airway obstruction or severe obesity (weight exceeding 200% of ideal for height) and pre‐treatment sleep studies do not demonstrate any evidence of sleep apnoea. Specific medical or surgical interventions for hyperinsulinism or Cushing’s syndrome will also lead to significant weight loss.

When to involve a specialist centre

  • Children with suspected hypothalamic tumours or endocrine causes of obesity should be managed in consultation with centres with expertise in the relevant neurosurgical investigations and paediatric endocrinology.
  • Children with obesity of such severity that significant adverse cardio‐respiratory consequences are suspected may need referral to a specialist unit for a detailed cardiorespiratory assessment, including sleep studies.
  • Children with sufficiently severe obesity that drug treatment or surgery is to be considered should be referred to a specialist centre for further evaluation.

Future developments

  • High‐quality randomized controlled trials of lifestyle interventions which aim to prevent or treat obesity in childhood by altering eating behaviour or patterns of physical activity are required.
  • A clarification of the role and benefits of pharmacological interventions in obese children.
  • An evaluation of the risks and benefits of surgery to treat childhood obesity.
  • Clarification of the value and ideal structure of an ‘obesity service’.
  • Further research should clarify the role and relationship between the multiple neurotransmitters known to influence hypothalamic function in the hope that a compound will be discovered which may have a significant effect on satiety without adverse side effects.


Obese teenage patients who have significant comorbidities, such as type 2 diabetes or other metabolic abnormalities or those experiencing significant adverse effects on cardio‐respiratory function, will require referral to adult services in their mid‐to‐late teenage years. Seeing these patients in a joint clinic staffed by both adult and paediatric specialists may be especially helpful to the paediatrician as it is likely that his/her adult colleagues will have much greater experience of a range of therapeutic interventions relevant to the management of the obese individual, some of which may be of value in the teenage age group.

Controversial points

  • How extensively should tall, obese children with no dysmorphic features be investigated?
  • How relatively important are genetic and environmental risk factors for obesity in childhood?
  • What is the future risk of obesity in adult life for an obese young child?
  • Is childhood‐onset obesity a risk factor for adverse metabolic consequences in adult life, independent of the presence of obesity in adult life?
  • Are children who become obese, less active than those who do not?
  • Do children from obese families, who are at increased risk of obesity, have an inherited decrease in their metabolic rates?

Potential pitfalls

  • Failure to recognize the diagnostic importance of distinguishing between obese children who are growing fast and those who have decreased linear growth.
  • Excessive and unrealistic expectations of the likely success of interventions to treat childhood obesity, especially when both parents are already obese.
  • Over‐investigation for a non‐existent pathological cause of obesity in an otherwise well, rapidly growing child.
  • Encouraging obese children to achieve dramatic short‐term weight loss is unlikely to be successful in achieving satisfactory regulation of longer‐term weight.
  • Excessive weight loss may lead to impaired growth.
  • Delayed diagnosis of type 2 diabetes or its misdiagnosis as type 1 diabetes in an obese child with minimal symptoms and absence of ketonuria when hyperglycaemia is finally documented.
  • Failure to diagnose clinically significant disturbances of respiratory function during sleep.
Aug 9, 2020 | Posted by in ENDOCRINOLOGY | Comments Off on Obesity
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