Essay: Childhood obesity

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DEFINITION:

Obesity occurs when more calories are consumed than are expended over time. Children < 2 years age: Obesity is defined based on weight for length for children <2 years age. The sex-specific weight for supine length ≥97.7th percentile on the World Health Organization (WHO) charts (1) is defined as Obesity.

Children > 2 years: In children ≥2 years old and adolescents a BMI >95th and 97th percentile is considered over-weight and obese respectively. Cut offs for overweight, obese and extremely obese are given in Table 1.

TABLE1
Overweight Obese Extremely Obese
BMI as per IAP BMI charts (5-18yr) ≥23 adult equivalent
Percentile:
boys-71st
girls-75th ≥27 adult equivalent percentile:
boys-90th
girls-95th

BMI percentiles as per 2000 CDC charts (2-20yr) ≥85th to <95th ≥95th ≥120% of 95th
Weight for length as per WHO charts (<2yr)
− ≥97.7th percentile

Assessment of obesity and predictive factors:
Assessment of obesity is done on the basis of BMI calculated by weight/height in m2 and plotting it on a BMI chart. Unfortunately this parameter cannot take into account the lean muscle mass of an individual. Muscular children may also have a higher BMI and racial/ethnic differences have been found in the fat content of individuals with the same BMI. On the other hand 25% children with a normal BMI have excess body fat. The risk of obesity related complications would be lower in children with higher muscle mass than in those with higher adiposity. Higher fat content and its distribution, especially central adiposity correlate better with the risk of obesity related complications. Hence Waist circumference may be a better parameter for predicting complications. Since measuring WC can be tedious for Pediatricians and most children with high BMI do have excess body fat, BMI should be used for assessing obesity.
BMI charts:
IAP Charts: BMI charts for Indian Children 5 to 18 years age were updated in 2015. The 23 and 27 adult equivalent cut offs lines (for risk of overweight and obesity, respectively) are similar to the IOTF cut-offs and are more appropriate for use in Asian children since they are known to have more adiposity and increased cardio-metabolic risk at a lower BMI (2). Hence it is preferable to use Indian IAP charts for our population 5-18years, WHO BMI charts from 2-5yrs age and weight for height charts by WHO for children <2 yrs age.
CDC charts: Children and adolescents ≥2 years of age are diagnosed as overweight if the BMI is ≥85th percentile but <95th percentile and obese if the BMI is ≥95th percentile for age and sex on the revised 2000 CDC charts. Extreme obesity is defined as a BMI ≥120% of the 95th percentile or ≥35 kg/m2 (3). WHO BMI charts are also available for children <5years of age.
The natural course of BMI in children shows a rise in the first year of life, followed by a fall and then a second rise at around 6 years of age, known as rebound adiposity. It has been observed that if rebound adiposity occurs at a lower age, the chances of adult obesity increase. Another study suggests that BMI at 7 years of age predicts adult obesity (24 in review). Studies on predictive factors needs more research currently, but it is suggested that the focus of Pediatricians should be on prevention of obesity rather than treatment. (review article)

PREVALENCE AND EPIDEMIOLOGY:
Obesity has become the number one public health problem in the world and there is a rise in prevalence in developing countries. The number of obese 5 to 19 year olds rose more than tenfold globally, from 11 million in 1975 to 124 million in 2016. An additional 213 million were overweight in 2016. The number of overweight or obese children aged 0 to 5 years increased from 32 million globally in 1990 to 41 million in 2016. This suggests that onset of obesity at a younger age is becoming more prevalent.
Over the last decade there has been a growing concern regarding the increasing prevalence of overweight and obesity among Indian adolescents. Prevalence data of childhood overweight and obesity from 52 studies conducted in 16 States in India were analyzed by WHO Centres in India. The pooled data after 2010 estimated a combined prevalence of 19.3 per cent of childhood overweight and obesity which was a significant increase from the earlier prevalence of 16.3 per cent reported in 2001-2005 (4).
ETIOLOGY
Childhood obesity is a complex multifactorial disease caused by the interaction of genetic and environmental factors. The commonest form of obesity encountered is “Simple Obesity” that is due to environmental factors.

PATHOPHYSIOLOGY
Evidence suggests that obesity is a disorder of the energy homeostasis system, rather than simply arising from the accumulation of excess weight. Obesity, therefore occurs when energy intake is more than energy expenditure i.e. sustained positive energy balance.
The homeostatic pathway of energy balance consists of:
1) Afferent arm: conveys peripheral information on hunger metabolism, in the form of neural & hormonal inputs, to the hypothalamus
2) Central processing unit: consists of different areas within the hypothalamus. The ventromedial hypothalamus (VMH) integrates afferent peripheral signals; Lateral hypothalamic area (LHA) & paraventricular nuclei (PVN) serve as neurotransmitter system to alter neural signals for changes in energy expenditure & feeding.
3) Efferent arm: network of autonomic effectors, which regulate energy expenditure, storage & intake.

Disruption in any of these arms can alter energy intake or expenditure, leading to either cachexia or obesity.

Efferent output

The adipocyte hormone leptin, which circulates at concentrations proportional to body-fat content, plays an important role in the relationship between obesity and energy homeostasis. A deficiency of leptin causes severe hyperphagia and obesity, with physiological leptin replacement corrects both hyperphagia and obesity in leptin-deficient individuals. But most individuals with obesity have elevated plasma leptin levels, raising the possibility that common forms of obesity are associated with leptin resistance.

1. Lifestyle and diet:
Lack of physical activity is a major contributor to childhood obesity. Evolution of multimedia, television, internet, video-games are engaging the child in sedentary lifestyle. Parents are now more conscious about the academic performance of the child, as a result of which child’s physical activity is restricted.
According to NHANES III (1988-1994), the prevalence of childhood obesity is highest among children who watch television ≥4hours/day and lowest among those who watch ≤1hour/day.
A large randomized control trial by Robinson(5) compared two groups of children at similar public schools. One group received a 6-month classroom curriculum to reduce television, videotape, and video-game use, while the other group did not. Robinson found that compared to the control group, children in the intervention group had statistically significant decrease in BMI.

Aside from these lifestyle issues, eating patterns of children and adolescents have changed dramatically in the past few decades. The consumption of high calorie soft drinks and junk food has increased tremendously. Children who frequently eat fast food consume more total and saturated fat, more total carbohydrate and added sugars, less dietary fiber, less milk, and fewer fruits and vegetables than children who eat fast food infrequently.

2. Metabolic Programming:
It has been well established that the metabolic programming of an individual determines the risk of developing obesity. Evidence for this comes from studies in which adoptive children and identical twins brought up in different environments had a BMI similar to their biological parents/twin (6,7).
Other factors that contribute to the metabolic programming are:
-In utero environment or maternal nutrition
-Birth weight (Small or Large for gestation)
-Gestation (Term or preterm)

2. Social factors:
Social factors associated with obesity include neglect, abuse, and generally non-supportive home environments. Neglected children are nine times more likely to become obese than other children (8). Food provides comfort and therefore that eating serves as a compensatory mechanism for children who have survived traumatic experiences or who live in difficult environments.

3. Genetics:
The current epidemic of obesity clearly reflects the environmental and behavior changes during the past half century, but the genetic background remains important, especially in the severe forms of obesity. In the most recent published update, there were more than 430 genes, markers, and chromosomal regions associated or linked with human obesity phenotypes (9). The human obesity gene map reveals that loci affecting obesity related phenotypes are found on all human chromosomes except chromosome Y.
The potential implication of genetic factors in the development of obesity is well demonstrated by the description of monogenic forms of human obesity. The genes implicated in these forms of obesity are summarized in Table 2. MC4R mutations are the most frequent cause of monogenic human obesity, occurring in up to 4% of early-onset and severe childhood obesity (10,11).
Homozygous mutations of the leptin-melanocortin genes are often associated with other features, e.g. hypogonadotropic hypogonadism in leptin deficiency and red hair and hypocortisolism in POMC deficiency.
Genetic Syndromes associated with obesity include Prader-Willi, Bardet-Biedl, Berardinelli-Seip congenital lipodystrophy, Alstrom, Borjeson-Forssman-Lehmann, Cohen, Beckwith-Wiedemann, Carpenter Syndrome.

TABLE 2
Genetic Obesity Syndromes Developmental delay Inheritance
Prader Willi syndrome + AD
Albright hereditary osteodystrophy + AD
BDNF/TrkB deficiency + AD
SIM1 deficiency + AD
TUB deficiency + AR
Bardet-Biedl syndrome + AR
SH2B1 deficiency – AD
MC4R deficiency – AD/AR
KSR2 deficiency – AD
Alstrom syndrome – AD
Leptin receptor deficiency – AR
Leptin deficiency – AR
PCSK1 deficiency – AR
POMC deficiency – AR

4. Endocrine:
Endocrine disorders as a cause of obesity are rare and are associated with additional symptoms. Endocrine causes of obesity include Hypothyroidism,
Cushing syndrome, Pseudohypoparathyroidism, growth hormone deficiency, Acquired hypothalamic obesity. The distinguishing feature of endocrine causes of obesity is that stature and height velocity are decreased, whereas a normal or increased growth rate generally excludes endocrine causes.
Acquired hypothalamic obesity is a syndrome of intractable weight gain caused by hypothalamic damage from a tumor or its treatment with radiotherapy or surgery. Such patients may have adequate growth velocity even when GH deficient but have tumor-related signs and symptoms.
Pediatric obesity is also associated with early puberty and advanced skeletal development.
5. DRUGS:
Weight gain is an adverse effect of many psychotropic medications and a leading cause of non-compliance in children taking these drugs. Psychotropic drugs that cause weight gain include certain classes of antidepressants, antipsychotics, and mood stabilizers such as Lithium, tricyclics and mono-amine oxidase inhibitors (MAOIs), Clozapine, olanzapine, risperidone and quetiapine.
The antiepileptic drugs valproate, vigabatrin, gabapentin and carbamazepine have been shown to cause weight gain(12).
Other medications associated with weight gain are drugs that block serotonin 5-HT2, histamine H1, dopamine D2 receptors (13) and high-dose chronic glucocorticoid therapy.

HEALTH CONSEQUENCES OF OBESITY:
Obese children are at great risk for becoming obese adults and the risk doubles when at least one parent is obese. India has been announced as the Diabetic Capital of the World by WHO because of continuous rise in population with diabetes mellitus.

1. Type2 Diabetes Mellitus (T2DM):
Most patients with this form of diabetes are obese and Insulin resistance is considered the greatest risk factor for the development of T2DM in obese children. Criteria for diagnosis of pre-diabetes and diabetes as per American Diabetes Association (14) is as follows:

TABLE 3
HBA1C Fasting plasma glucose, mg/dl 2 hour plasma glucose during an OGTT, mg/dl
Pre-diabetes 5.7-6.4% 100-125 140-199
Diabetes ≥6.5% ≥126 ≥200

Fasting is defined as no caloric intake for at least 8 h. In patients with classic symptoms of hyperglycemia random plasma glucose of ≥200mg/dl is also labeled as Diabetes.
The American Diabetes Association recommends screening of children at risk of T2DM ie. those with a BMI ≥85th percentile and two or more of the following additional risk factors: affected first or second degree relative, member of a high-risk ethnic group that includes Asian Indians and signs of insulin resistance eg. Acanthosis nigricans, PCOS. Screening is performed at 10 years of age or at the onset of puberty (whichever occurs first) and every 3years thereafter (15). If any symptom of T2DM is noticed screening can be done earlier. HbA1C should not be used to screen for T2DM since the studies were performed in adults and it is not a reliable screening test in children and in certain races.

2. Dyslipidemia:
Norms for lipid profile in children (16) are different from adults and are given in Table 4

TABLE 4
Acceptable, mg/dl Borderline, mg/dl Abnormal, mg/dl
Total cholesterol <170 170-199 ≥200
LDL Cholesterol <110 110-129 ≥130
Non HDL Cholesterol <120 120-144 ≥145
Triglycerides
0-9y
10-19y
<75
<90
75-99
90-129
≥100
≥130
HDL Cholesterol >45 40-45 <40

Children with dyslipidemia are at a higher risk of developing Metabolic Syndrome and consequently cardiovascular disease at a younger age. Hence identification and treatment of youth with dyslipidemia is of utmost importance. Fasting lipid profile should be done. If the S.cholesterol level is high, hypothyroidism should be ruled out.
Children with lipid abnormalities should be managed initially for 3 to 6 months with diet changes, increased physical activity, reduced screen time, and caloric restriction. Indications for pharmacotherapy in children with dyslipidemia are mentioned in chapter on lipid disorders in children.
3. Hypertension:
It is estimated that about 60% of pediatric patients with hypertension have essential hypertension. Among the patients with essential hypertension 75% are obese, thus the most common cause of pediatric hypertension is obesity. Definition of Pre-hypertension and hypertension is given below(16). White-coat hypertension is present when BP readings in health care facilities are greater than the 95th percentile but are normotensive outside a clinical setting. Any abnormal BP reading should be repeated twice by auscultation if performed with oscillometric device.

TABLE 5
Prehypertension Stage 1 Hypertension Stage 2 Hypertension
BP percentile for age & gender >90th to <95th ≥95th to <99th +5mmHg ≥99th +5mmHg

METABOLIC SYNDROME (MS)
Metabolic Syndrome is also known as syndrome X and is characterized by:
-Obesity (abdominal)
-Atherogenic dyslipidemia (elevated triglyceride [TG] levels, high low-density lipoprotein [LDL] particles, and low high-density lipoprotein cholesterol levels
-Raised blood pressure
-Abnormality of glucose metabolism (impaired fasting glucose or GTT)
-Prothrombic inflammatory vascular environment
The presence of this cluster of factors increases the risk of cardiovascular events.
Childhood obesity predisposes to endothelial dysfunction, carotid intimal medial thickening, and the development of early aortic and coronary arterial fibrous plaques. Sleep apnea and obesity related hypoventilation might contribute to pulmonary arterial hypertension.
MS has been a well-defined entity in adults but the definition in children is still variable. Prevalence rates in the pediatric age group vary depending on the criteria used.

The International Diabetes Federation’s (IDF) criteria (17) for diagnosing metabolic syndrome requires the presence of central obesity plus any two of the other four factors:

TABLE 6
10 to <16years ≥16years
Obesity (WC)* ≥90th percentile ≥94cm (males)
≥80cm (females)
Triglycerides ≥150mg/dl ≥150mg/dl
HDL cholesterol <40mg/dl <40mg/dl (males)
<50mg/dl (females)
Blood Pressure SBP ≥130mmHg, or
DBP ≥85mmHg SBP ≥130mmHg, or
DBP ≥85mmHg, or
Treatment of previously diagnosed Hypertension
Fating plasma glucose ≥100mg/dl, or
known T2DM ≥100mg/dl, or
known T2DM
*Country specific waist circumference standards should be used if available.

For children aged 6 to <10yr, though MS cannot be diagnosed but further measurements should be made in children with a family history T2DM, MS, dyslipidemia, cardiovascular disease, hypertension and/or obesity.

NCEP/ATPIII definition for children 12-18 years: Individuals with ≥3 of the following are considered at risk for MS:
-Waist circumference ≥90th Percentile for age and sex
– HDL cholesterol ≤40 mg/dl,
-Triglycerides ≥110 mg/dl
– Fasting plasma glucose >110 mg/dl, and
-BP ≥90th percentile according to age and sex
Waist circumference percentiles for the Indian Population were published recently by Khadilkar et al (18). They have suggested a cut-off of 70th percentile for WC, to screen for Metabolic Syndrome in Indian children.

5. Nonalcoholic Fatty Liver Disease (NAFLD):
Nonalcoholic fatty liver disease (NAFLD) constitutes a spectrum of conditions, ranging from steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis, in the absence of excessive alcohol consumption. The prevalence of NAFLD is 34.2% in obese children & adolescents and the reported prevalence is highest in Asia (19).
Most children are asymptomatic, while some may complain of right upper quadrant pain or abdominal discomfort. NAFLD aggravates hepatic insulin resistance, thereby increasing the risk of developing T2DM.
The liver SAFETY (Screening ALT for Elevation in Today’s Youth) study was conducted to develop ALT thresholds and the cut-off of ALT >25 for boys and >22 for girls were suggested for screening NAFLD in children (20).

6. Polycystic Ovary Syndrome (PCOS):
Increased adiposity, especially abdominal, is associated with hyperandrogenemia and increased metabolic risk. The diagnosis of PCOS in an adolescent girl should be made based on the presence of clinical and/or biochemical evidence of hyperandrogenism (after exclusion of other pathologies) in the presence of persistent oligomenorrhea (21). Polycystic ovary morphology on ultrasound is not reliable to make a diagnosis in adolescents because multi-follicular ovaries are a feature of normal puberty that subsides with onset of regular menstrual cycles (22).

7. Psychiatric:
Results from several studies suggest a higher rate of depression among obese children than among children of normal weight. In addition to depression, anxiety and low-self esteem have also been found to relate to obesity in children and adolescents. A study by Grilo et al. (23) demonstrated that “the greater the frequency of being teased about weight and shape while growing up, the more negative one’s appearance is regarded, and the greater the degree of body dissatisfaction in adulthood”.

8. Miscellaneous:
Orthopedic problems, such as slipped capital epiphyses and Blount’s disease, occur in obese children. Approximately 50% to 70% of children with slipped capital epiphyses are obese. Obese children are also at a higher risk for developing gall stones, pseudotumor cerebri and obstructive sleep apnea.

EVALUATION OF THE OBESE CHILD:
Obese children often present to the Pediatrician/pediatric Endocrinologist with a concern about a hormonal cause of obesity or secondary to consequences of obesity eg. Concern about gynecomastia or embedded penis in males(pic1), irregular periods, acne or hirsutism in females and acanthosis nigricans(pic2) in both sexes.
A detailed history and physical examination is in order to elicit any cause of obesity and evaluation of consequences should be done depending on the age and degree of obesity.
1) History: It is a crucial part of evaluation of obesity and leading questions should be asked to elicit a cause as well as consequences of obesity.
A detailed history should be obtained regarding the onset (infancy/childhood), duration as well as the rapidity of weight gain. Infantile onset of obesity points towards a possibility of monogenic obesity.
A recent increase in appetite with rapid weight gain could suggest and intracranial mass especially if it is associated with headaches or visual disturbances.
Antenatal history and Birth weight are important in predicting the risk of complications. Children born small/large for gestation and those born to mothers with gestational diabetes mellitus have a higher risk of developing Type 2 Diabetes Mellitus.
History of developmental milestones may give a clue to the cause of obesity eg. Delayed motor milestones, feeding difficulty in infancy followed by a voracious appetite may be suggestive of Prader-Willi Syndrome.
Family history of obesity, diabetes mellitus, hypertension and dyslipidemia should be obtained.
History of intake of antipsychotics, anti-depressants or long-term corticosteroids should be obtained as they lead to weight gain.
Polyuria, polydipsia and unexplained weight loss may suggest onset of diabetes mellitus. Scanty and Delayed or missed periods in girls with or without hirsutism may suggest the presence of polycystic ovarian disease (PCOD).
Enquire about excessive daytime sleepiness, snoring and morning headaches for obstructive sleep apnea and knee or hip pain for Slipped capital femoral epiphyses.
History of dietary practices, TV/screen viewing duration and physical activity may give some insight into the cause of weight gain. Majority of parents of obese children feel that their child’s weight gain is due to pathology and are oblivious to their life-style. A detailed dietary history with calculation of caloric intake would help convince them about the need for life style changes.

2) Anthropometry:
Obtain a weight, height, calculate BMI and measure waist circumference (WC) if possible. Plot these measurements on respective charts for age and gender for the Indian population.
BMI chart will classify the child as over-weight/obese and demonstrate the duration and rapidity of weight gain.
Reduced height velocity suggests an endocrine problem whereas in exogenous obesity linear growth is normal.
Waist Circumference (WC) is a good indicator of central adiposity and is a better predictor of metabolic syndrome (24,25), cardiovascular disease risk factors (26) and insulin resistance in children than BMI.
A cut-off of 70th WC percentile is suggested to screen children for risk of MS in our population. WC is measured with the child standing using a non-stretchable tape applied horizontally just above the upper lateral border of the right ileum(27). Measurement is made at the end of a normal expiration and recorded to the nearest 0.1cm. Age- and sex-specific reference curves for WC for 2-18 year old Indian children are available by Khadilkar et al (18).

3) Clinical Examination:
This includes assessment of vital signs especially measurement of Blood pressure with an appropriate size cuff.
Look for dysmorphic features that would suggest a genetic syndrome. Cushingoid facies, hyperpigmented stretch striae and hypertension suggest cushing’s or exogenous steroid exposure. A hump on the back of neck and stretch striae may also be present in children with simple obesity. Dry skin or enlarged thyroid gland may suggest hypothyroidism and presence of acanthosis nigricans is an indicator of insulin resistance. Acne and hirsutism in girls could be due to PCOD. Shortening of 4th and 5th metacarpal should raise the suspicion of pseudohypoparathyroidism.
Look for gynecomastia in males. Genital examination for Tanner staging & evaluation of early puberty should be done. Undescended testes in males could be associated with syndromic obesity.

4) Laboratory Investigations:
Initial investigations include evaluation for cause and consequences of obesity. Specific testing for the endocrine disorders is done only if there is strong clinical suspicion. These are mentioned in Table 3. Genetic testing should be considered in children with early onset severe obesity, voracious appetites, family history of severe obesity and in those where a clinical suspicion of genetic obesity syndromes is present. Lab investigations currently available in India for monogenic obesity are; MC4R, Leptin and FTO gene. Leptin deficiency is rare and resistance is more common. TSH levels are often mildly elevated in obese children and are a major cause for referral.

TABLE 7: Diagnostic evaluation for cause of obesity
Disease suspected Investigation
Hypothyroidism FT4, TSH
Cushing disease Urine free cortisol
S. cortisol: Morning & Evening
GH deficiency IGF1 & IGFBP3
GH stimulation test
Genetic syndromes DNA methylation: PWS
CNS disorder MRI brain
Monogenic obesity MC4R gene testing
Leptin levels

Fasting lipid profile, HBA1C, SGPT and Fasting plasma glucose should be checked in all over-weight and obese children after 3 years of age.
An Oral Glucose Tolerance Test (OGTT) should be performed in obese children with a family history of T2DM as per guidelines mentioned in above section and in grossly obese children.
Although obesity is associated with insulin resistance, diagnosis of insulin resistance by measuring plasma insulin concentration is no longer recommended, since the insulin assay is unreliable. ALT level greater than 25 and 22 in males and females respectively warrants ultrasonography of the liver followed by biopsy in those with a suspicion of cirrhosis.
TABLE 8
HISTORY
Mental retardation Genetic etiology
Short stature/ decreased height velocity Endocrine etiology
Medication history, eg. antipsychotics Medication etiology
Snoring, morning headaches Obstructive sleep apnea
Knee or hip pain Orthopedic morbidity
Polyuria, polydipsia Type 2 Diabetes
Hirsutism, irregular menses PCOS

PHYSICAL EXAMINATION
Dysmorphism Genetic syndromes
Acanthosis nigricans Insulin resistance
BP ≥95th percentile Hypertension
Hepatomegaly Hepatic steatosis
Tanner staging Early puberty
Papilledema Pseudotumor cerebri
Hirsutism PCOS

MANAGEMENT
Comprehensive interventions combining diet, physical activity, education, and behavioral therapy are associated with improvement in terms of weight reduction and metabolic outcomes. The Expert Committee on Obesity Evaluation and Treatment recommends that the primary goal should be developing healthy eating and activity habits, not achieving ideal body weight. The environment that shapes behavior of the child should be modified and family influence is the most important factor in childhood obesity treatment. For weight loss, obese children must expend more energy than they consume, by decreasing caloric intake and increasing physical activity. Studies show interventions involving exercise alone did not cause weight loss but when exercise was combined with diet and education, reduction in body weight was noted.
Consumption of fast food in children has increased over the past few years because of the easy availability and media marketing. Fast foods (eg. Pizza, burger, fries, somosa, pakora, potato chips, soft drinks, etc) have high level of fat and sugars that are unhealthy but addictive, making it hard for children to choose healthy food. Nutrition labeling might restrict the quantity and choice of food among children of educated parents. In a recent study conducted on parents of children aged 3-6 years, showed that labeled menus lead to significantly lower calorie content in restaurant meals purchased for children (28).

The American Academy of Pediatrics (AAP) suggests a staged approach to pediatric weight management:
TABLE 9
1. Prevention plus
• Encourage consumption of ≥5 servings of vegetables and fruits daily.
• Minimize beverages with sugar (eg; soda, sports drinks).
• Eat healthy breakfast everyday
• Prepare more meals at home
• Eat at the table as a family at least 5-6 times/week and involve the whole family in lifestyle changes.
• ≤ 2hours of screen time per day (no television viewing for children <2yr old)
• ≥ 1hour of physical activity daily
• Reinforce goals at each healthcare visit
• Allow child to self-regulate his/her meals and avoid overly strict eating regimens.
2. Structured weight management
• Structured daily meals and planned snacks with balanced macronutrients (breakfast, lunch, dinner, and 1 or 2 scheduled snacks, with no food or calorie containing beverages at other times)
• Emphasize food with low energy density (those with high fiber or water content)
• Reduce frequency and quantity of foods with high energy density (eg; fried foods, baked goods, fats)
• Limit portion size
• Set explicit behavior goals ≤ 1hour of screen time daily
• ≥1hour of physical daily, supervised
• Monthly patient-provider contact
• Monitor eating & physical activities through logs
• Use positive reinforcement techniques (reward system)
• Strong parental involvement for school aged children
3. Comprehensive multidisciplinary intervention
• Same as stage 2, along with structured diet & physical activity designed for negative energy balance behavioral interventions like development of short-term diet & physical activity goals.
• Weekly patient-provider contact (and/or phone) for a minimum of 8-12 weeks. Subsequently, monthly visits can help maintain new behaviors.
• Parent training in behavioral techniques to improve home eating & activity environment

4. Tertiary care intervention
• Used for severely obese children who failed in comprehensive multidisciplinary intervention stage but are willing to maintain physical activity and healthy diet. Options include pharmacotherapy and bariatric surgery but children should be carefully selected for this intervention and only is absolutely required.

If there is no improvement after 3-6 months of stage1 adaptation, the patient can move on to stage 2. Similarly after 3-6 months in a structured weight management program, some patients who have not achieved goals can move to stage 3.
TABLE 10
Age Weight goals according to BMI percentiles
2-5y 85-94th: weight maintenance until BMI is <85th percentile, or slowing of weight gain as indicated by lowering of BMI
≥95th: weight maintenance until BMI is <85th percentile (weight loss of up to 0.5kg/month is acceptable)
6-11y 85-94th: weight maintenance until BMI is <85th percentile, or slowing of weight gain as indicated by lowering of BMI
95-99th: gradual weight loss (0.5kg/month)
>99th: weight loss (maximum 1kg/week)
12-18y 85-94th with no health risks: weight maintenance
85-94th with health risks: weight maintenance or gradual weight loss
95-99th: weight loss (maximum is 1kg/week)
>99th: weight loss (maximum is 1kg/week)

For infants, exclusive breastfeeding should be encouraged till 6months of age and continue breastfeeding after introduction of solid food till 12 months of age and beyond. Sugar sweetened beverages should be avoided in infants and there should be not television in the infant’s sleeping room.
For overweight/obese 12-24months old children, healthy diet and age appropriate physical activity is recommended. Three major meals should include healthy food, with plenty of fruits & vegetables. Fruit juices and sugar-sweetened beverages should be avoided. No television viewing during meals and overall screen time should be limited.
MARG intervention study (29) conducted in India aimed to evaluate the impact of a school-based health and nutritional education program on knowledge and behavior of Indian school children. They educated 40196 children (aged 8 – 18 years), 25000 parents and 1500 teachers about health, nutrition, physical activity, non-communicable diseases and healthy cooking practices in three cities of North India (New Delhi, Agra, Jaipur) during the period August 2006 to December 2008. Major gaps exist in health and nutrition-related knowledge and behavior of Indian children, parents and teachers. Following the intervention, scores improved in all children and a significantly higher improvement was observed in younger children (aged 8 – 11 years) as compared with those aged 12 – 18 years, and in females compared with males. This successful and comprehensive educative intervention could be incorporated in school-based health and nutritional education program.
Medical complications associated with weight loss include inadequate nutrient intake and slow linear growth, therefore eliminating only high-calorie foods and encouraging well-balanced eating minimizes the risk of inadequate nutrient intake.
Obesity is a chronic disease and improvement decreases once treatment stops, so children and parents must work actively to maintain behaviors that promote weight loss. Regular contact with the clinician is essential to reinforce treatment goals and skills.
Pharmacotherapy
Pharmacotherapy for children or adolescents with obesity is used only if intensive lifestyle modification has failed to stop weight gain or to ameliorate comorbidities. Use of medication should not be the only mode of treatment in obese children. Only one drug is approved for use in children for weight loss.

TABLE 11
Drug Mechanism of action Side effects Other uses
Orlistat FDA approved for ≥12years of age Inhibits gastric & pancreatic lipases, resulting in reduced absorption of fats Fatty/oily stool, abdominal cramps, fecal incontinence, reduced absorption of fat soluble vitamins
Metformin not FDA approved for treatment of obesity Reduces hepatic glucose production, decreases intestinal absorption of glucose & increases peripheral insulin sensitivity GI complaints, nausea/vomiting, vitamin B12 deficiency, lactic acidosis (rare) Approved for ≥10 years of age for treatment of T2DM, metformin could also be used to regulate menses in obese girls with PCOS

Other drugs used only in certain special situations are:
• Growth hormone: Prader Willi syndrome
• Octreotide: Hypothalamic obesity
• Leptin: Leptin deficiency
The FDA approved a number of weight-loss medications for adults and these medications are appropriate for those ≥16 years of age with BMI ≥30kg/m2 or who have BMI ≥27 kg/m2 and at least one weight related comorbidity (e.g., hypertension or T2DM).
Medication should be discontinued and the child should be re-evaluated if he/she does not have a 0.4% BMI/BMI z-score reduction after taking full dose of anti-obesity medication for 12 weeks.
BARIATRIC SURGERY
Pre-requisites (Endocrine Society recommendations):
1) Adolescent Tanner 4-5, and final/near final adult height.
2) BMI 40kg/m2 or BMI >35kg/m2 and significant extreme comorbidities.
3) Extreme obesity and co-morbidities persist despite lifestyle modification, with or without trial of pharmacotherapy.
4) Psychological evaluation confirms stability & competence of the family
5) Patient demonstrates ability to adhere to the principles of healthy dietary and activity habits.
6) Access to experienced surgeon in medical center.

Contraindications of bariatric surgery: preadolescents, pregnant/ breastfeeding, unresolved eating disorder, untreated psychiatric disorder, or Prader-Willi syndrome.

PREVENTION

Lifestyle behaviors to prevent obesity, rather than intervention to lose weight should be aimed in all children. Efforts must begin early in life, because childhood obesity usually persists into adulthood. Exclusive breastfeeding should be encouraged till 6months of age and maintenance of breastfeeding after introduction of solid food till 12 months of age. Children should limit consumption of sugar-sweetened beverages and fast foods, limit screen time, and consume well balanced diet. Consumption of whole fruits should be encouraged rather than fruit juices. Children and adolescents should engage in at least 20 minutes, ideally 60 minutes, of vigorous physical activity at least 5 days per week to improve metabolic health and reduce the chances of developing obesity. Participation of the parents to help the child develop healthy eating habits is crucial to prevention of obesity.

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