ADOLESCENT'S OBESITY
Dr. Vaman Khadilkar*
Paediatric & Adolescent Endocrinologist, Bombay Hospital, Mumbai Deenanath Mangeshkar Hospital & Jehangir Hospital, Pune.*
Introduction
World Health Organization has declared obesity as one of the most neglected disease of significant public health importance of this century.(1) Obesity has reached epidemic proportions in the developed part of the world with as many 30-40% of adults being already obese and the incidence in children and adolescent is rising. In the United States the prevalence of children and adolescents with Body Mass Index of greater than 95 percentile has doubled in the last 2 decades and there is 50% increase in the prevalence of those with a BMI of greater than 85 percentile.(2) Obesity is increasingly reported from countries that have acquired affluence in the recent times such as Taiwan and Saudi Arabia. (1) The incidence of obesity at all ages is on the rise in the developing countries including India, as well. In a study done by Dhurandhar et al in 1993 in Mumbai, the incidence of obesity in adults was found to be as high as 30-40%. (3)

Obesity in children and adolescent is more dangerous than adulthood obesity because it has more devastating health consequences. It is also extremely frustrating to treat and multidisciplinary approach along with active participation from the family, school and even society as a whole is necessary. Research into the etiology, prevention and treatment has unfortunately not taken major strides into lifestyle disease of major public health importance which is showing an alarming rise in incidence around the world.
Definition
Obesity is increased body fat. Many definitions of obesity have been proposed based on body weight, weight for height, percentage of ideal weight for age and body mass index (BMI). Weight alone is not a good index of fatness as it does not consider height. Weight for height is also not perfect, at it does not differentiate between muscles mass and fat mass. BMI is the currently accepted method of diagnosing and grading obesity. BMI is given by the formula, weight in kg upon height in meters squared. A body mass index of more than 25 is OVERWEIGHT and more than is OBESE by internationally accepted definitions in ADULTS.(1) In children and adolescent, no such definition is appropriate and hence BMI percentile charts are used. These percentile charts cannot be universal and have to be country and population specific. In children BMI above 85 percentile for any age is OVERWEIGHT and above 95 percentile is OBESE. It is also observed that Indians have more body fat as compared to their Caucasian and black counterparts at a given BMI. (4) Various methods for accurate measurement of body fat are available and include underwater weighing, plethysmography, electric impedance, Dual Energy X-ray absorptiometry (DEXA) and skin fold thickness measurements with a caliper. All these methods although very useful for research purpose are cumbersome and inconvenient to use in clinical practice. Therefore, the clinical evaluation of obese children and adolescent upon calculation of BMI percentile for children and adolescents are not yet available.
Etiology and Epidemiology
In India, the incidence of childhood obesity is on the rise and Kapil et al reported an incidence of 30% amongst in an affluent school in Delhi between the ages of 8 and 15 years. (5) Author's own studies in Pune, Maharashtra have shown an incidence of overweight children to be 15-30% in English medium schools and <1% in corporation schools (Unpublished data).

Majority of cases of childhood and adolescent obesity is caused by excessive calorie intake often coupled with reduced physical activity. High calorie food consumption resulting from wrong food choices such as "fast food ", low fiber diet and copying Western food style is seen more and more commonly in the developing world. Urbanization, poor road safety, use of automobiles, excessive television viewing and prolonged school hours has all added to reduced physical activity. This combination of excessive calorie intake along with sedentary lifestyle is the main cause of obesity epidemic that is being witnessed by the developed as well as developing countries like India.

Defects of the endocrine system can cause obesity in children and adolescent, but this is seen in only a small minority of cases. Primary endocrine diseases causing obesity is rare and includes: Hypothyroidism, Cushing syndrome and Growth hormone deficiency. Secondary hormonal changes such as impaired glucose metabolism, insulin resistance and polycystic ovarian syndrome are not uncommon in obese adolescents but they are an effect and not the cause of obesity.

Proponents of genetic theory in the pathogenesis of obesity have shown that there is difference in the handling of calorie load amongst different individuals and that explains the varying severity of obesity seen in different individuals receiving the same calorie load. Leptin and Ob gene defects that are extremely rare also cause severe obesity. (6) Although obesity may rarely be caused by identifiable genetic defects in some individuals, its unlikely that a genetic shift in the whole world's population is the cause of present day epidemic of obesity. It is more likely to be a combined effect of the profound change in eating habits and severely reduced physical activity caused by changing lifestyle due urbanization around the world.(1) Rare syndromic causes of obesity include Prader-Willi syndrome, Lawrence Moon Biedl syndrome, Carpenter syndrome, Alstrom syndrome and Cohen syndrome.
Pathogenesis
Positive energy balance leads to conversion of excess calories into fat, which gets deposited in the areas where adipose tissue normally lies such as the subcutaneous area, omentum, peritoneum and even within the muscles and liver. The distribution of fat can be different in different races and individuals and Indians tend to have more visceral fat. (7) Depending upon the pattern of adiposity, two distinct types namely, android and gynecoid have been defined. In the android variety, fat deposition is mainly in the abdominal area and in the viscera whereas in the gynecoid type it is mainly over buttocks and thighs. As the adiposity increases individuals tend to become insulin resistant particularly when they have a genetic predisposition. If an individual is born small for gestational age he is likely to be more insulin resistant due to fetal programming and hence is more prone to develop type 2 diabetes, coronary heart disease, stroke and hypertension. (8) Adipose tissue has an enzyme called aromatase, which is a bi-directional enzyme that converts estrogen into androgen, and vise a versa. This enzyme plays a role in the causation of gynecomastia in boys and functional hyperandrogenemia in obese girls. In obese girls, insulin resistance and increased androgens contribute to the development of polycystic ovary syndrome (functional ovarian hyperandrogenemia).
Investigations
Investigations of an obese child or adolescent starts with detailed anthropometric examination and calculation of anthropometric indices and accurate blood pressure measurement.
  1. Early morning (8 am) estimation of cortisol to rule out Cushing's syndrome, thyroid function tests and in the presence of family history of diabetes or clinical of evidence of acanthosis nigricans an oral glucose tolerance test with 1.75 gm per kg glucose load along with insulin values
  2. Low dose dexamethasone suppression test is necessary when initial cortisol value is high. It is not unusual to find high cortisol values in patients with simple obesity. Theses values however are readily suppressed with low dose dexamethasone.
  3. Testosterone, 17 hydroxyprogesterone, prolactin and LH, FSH in the first week of menstrual cycle in cases where obesity is associated with hirsutism or rather features suggestive of PCOD.
  4. Lipid profile
  5. Growth hormone stimulation test if clinical signs of growth hormone deficiency such as short stature and truncal obesity are present.
  6. Chromosomal analysis and specific genetic probe studies in syndromic obesity.
Treatment
Except in cases endocrine obesity, the mainstay of treatment is diet, exercise and behavior modification. As majority of obesity seen in adolescents is nutritional, dietary restriction (30 to 40% of calorie deficit for the age per day) is administered making sure that child receives enough proteins. A diet high in fiber, complex carbohydrate and low in fat is recommended. The diet allows adolescents to loose weight at a speed of about 0.5 kg per week and still allows them to grow at normal speed.

In case of morbid obesity, protein sparing modified fast (PSMF) is recommended in which only about 700-900 calories per day are allowed again making sure that sufficient protein (1.5-2.5 gm/kg/day) is given. Adolescent needs education in the correct choice of food.

Behaviour modification therapy is found to be beneficial in some patients. Students have shown positive effect on weight loss by group therapy in which exercise and dietary therapy is given to group of adolescents. (9)

Pharmacotherapy for obesity in children and adolescents is being evaluated and studies are under way but at present no medication is routinely used in clinical practice.

Metformin (insulin sensitizer), sibutramine (CNS dopaminergic agent), orlistat (Intestinal lipase inhibitor) are being evaluated with some studies showing a definite positive effect on weight loss.(2) Leptin in leptin deficient individuals (very rare) has shown a very good response, however, it has shown variable response in leptin sufficient individuals (6). Newer pharmacological agents such as those acting on neuropeptide Y, melanocortin 4 receptor (glucagon like peptide 1), orexins and uncoupling proteins on mitochondria are being studied with not much data available at this stage.(10)

Bariatric surgery (in which capacity of the stomach is reduced) is reserved for extremely obese adolescents with a BMI above 35 and associated co-morbid factors such as dyslipidemia, hypertension, sleep apnea, etc. It is very important to make the patient realize that there is "No magic bullet to reduce weight rapidly and there is no alternative to diet, exercise and change of lifestyle."

The treatment of endocrine obesity depends upon the type of endocrinopathy. In case of primary hypothyroidism, thyroxin replacement therapy is given in a dose varying from 25 to 200 mcg per day depending upon the weight of patient, clinical response and biochemical parameters. In Cushing's syndrome, treatment is directed at the source of the problem such as removal of removal of adrenal or pituitary mass. Growth hormone deficiency needs treatment with recombinant human growth hormone.

Conclusion: Obesity has reached epidemic proportion around the world including India and is seen at a younger and younger age. The incidence of obesity in the developing part of the world including India is rising. Obesity in childhood and adolescents is a more serious disease than in adults with far reaching health consequences. In the majority of patients, obesity is caused by a combination of excessive calorie intake and sedentary lifestyle. There is no magic bullet to treat obesity. Diet and exercise remains the mainstay of treatment. Medications and bariatric surgery are reserved for the most severely obese and resistant cases with BMI above 30 and associated risk factors.
References :
  1. OBESITY EPIDEMIC PUTS MILLIONS AR RISK. WHO.1997;46.
  2. Styne DM. Childhood and adolescent obesity, Prevalence and significance. PCNA 2001;48:(4):823-54.
  3. Dhuradhar NV, Kulkarni PR. Prevalence of obesity in Bombay. Int J Obes Relat Metab Disorders 1992;16(5):367-75
  4. Deurenberg P, Deurenberg- Yap M, Schouten FJ. Validity of total and segmental impedance measurements for prediction of body composition across ethnic population groups. Eur J Clin Nutr 2002;56(3):214-20.
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