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CHILDHOOD OBESITY
 

Childhood obesity has emerged as a major health hazard of the twentieth century with significant

impact on the health of the community at large. The incidence is rising in our country, thanks to urbanization,

sedentary life styles and availability of processed, calorie dense foods. This article is aimed at providing an

outline for the assessment, workup and management of this very challenging problem.

Childhood obesity by definition is excessive storage of energy as fat relative to lean body mass.

 
 

Precise assessment can be difficult. The methods available are:

1. Body Mass Index (BMI): weight in kg/ (height in m)2 This has limited application in overweight growing

children, since BMI is based on stable height.

2. Age specific growth charts: The advantage is the ability to compare the prior growth pattern; the

disadvantage is not taking into account frame size and body composition.

3. Weight greater than 120% (relative weight for height): does not differentiate fat weight from muscle and

bone weight, but is a useful office tool and quite reliable.

4. Skinfold thickness: can be very useful as a gauge for adiposity. It is fraught with methodological difficulties,

but can be combined with other methods for monitoring weight loss.

5. Waist hip ratio (WHR) is an important parameter to assess, but less useful in children as age-related data is

not available.

6. CT, MRI, Ultrasound & Dexa are available to quantitate fat tissue, but are not useful for routine clinical

practice.

A combination of WHR, relative weight for height, and skinfold thickness could be ideal simple office

assessment methods.

Pathophysiology: Besides evidence for inheritance of human obesity (twins, adoptee studies) and other specific

causes of weight gain (hypothalamic tumors, thyroid dysfunction, insulin resistance etc.), the new biology of

obesity with the discovery of leptin has generated tremendous interest and optimism. Leptin is a protein coded

by the ob gene, which is secreted by adipose tissues, circulates and enters the CSF and binds to the

hypothalamus. Also, circulating levels of leptin are high in obese humans, similar to insulin resistance.

However, defects in the ob and leptin receptor gene in obese individuals are not apparent yet. It has been

postulated and proved that leptin produces satiety. Studies testing the application and therapeutic utility of leptin

are in progress.

 
 

Health Consequences:

1. Obesity in adulthood

2. Hypertension

3. Type II diabetes mellitus

4. Hyperlipidemia

5. Accelerated atherosclerosis

6. Gall bladder disease

7. Bone and joint deformities

8. Gout

9. Hyperinsulinemia

10. Psychosocial problems (negative stereo-typing, poor peer acceptance)

11. Increased mortality in adulthood, independent of adult weight

12. Cancers

Causes of obesity

1. Genetic factors: This could be a function of genetically determined resting energy expenditure, maternal

obesity, low basal metabolic rate, or an inherited dysmorphic form of obesity. Syndromes such as Prader Willi,

Carpenter, Lawrence Moon Beidl, Cohen and Alstrom, have characteristic features that help identification.

Studies of twins and adopted children have further validated the "genetic" theory.

2. Environmental factors: such as birth weight, maternal weight, maternal diabetes, excessive feeding during

infancy, inactivity, male sex and television viewing have been implicated.

3. Dietary factors: High fat, high carbohydrate, calorie dense foods, frequent dieting (thereby lowering fat free

mass), and under-reporting of calorie intake are all contributing factors.

4. Hypothyroidism: leads to weight gain and poor height gain. Frequently looked for, it is an unusual cause for

childhood obesity.

5. Insulin resistance: characterised by obesity, acanthosis nigricans, menstrual irregularities, hirsutism, is often

seen in adolescent girls, and offspring of parents with type II diabetes mellitus.

6. Hypothalamic obesity: Destruction of the appetite/ satiety center in the hypothalamus due to tumors like

craniopharyngioma, infections, trauma, etc can lead to excessive weight gain.

7. Miscellaneous: Cushing syndrome, hypogonadism, Turner syndrome, Klinefelter syndrome, growth hormone

deficiency, are rare causes of obesity.

 
 

Workup:

1. History: Birth weight, growth pattern, feeding pattern, maternal weight, diabetes, appetite, thirst, complete

diet and activity history, family history of obesity.

2. Physical exam: Special attention to dysmorphic features, height, WHR, pubertal staging, clinical features

suggestive of thyroid/ adrenal/ pituitary dysfunction, acanthosis, hirsutism, all provide important clues to the

underlying disorder.

3. Psychologic assessment: Self esteem, body image perception, attitude towards food and exercise, school

performance, inter-personal relationships, attitude of parents and siblings, and peer acceptance, must be

documented.

4. Detection of complications of obesity: BP, lipids, bone and joint deformities (slipped femoral epiphyses,

genu valgum, tibia vara), hypoventilation syndrome.

5. Lab evaluation:

a. Fasting blood sugar (all)

b. Lipids (all)

c. Bone age (all)

d. T4, TSH (all, to rule out subtle deficiency)

e. Urine specific gravity (presence of thirst/ polyuria)

f. Androgens (presence of hirsutism + menstrual irregularities)

g. Fasting insulin with simultaneous sugar (presence of features of insulin resistance or hypoglycemia)

h. Imaging of sella (presence of excessive appetite, thirst)

i. Karyotype (+ce of dysmorphic features)

Management

The five modalities available are:

1. Diet: Low fat; small frequent meals, with low calorie snacks; avoidance of calorie dense foods ("junk" foods),

eating in front of TV, eating out. Increased intake of fruits, vegetables (especially salads), dals and skimmed

milk cuts down overall fat intake.

2. Exercise: walking, cycling, aerobics, playing outside, tennis, badminton, cricket are good activities.

Swimming leads to increase of appetite, which should be cautioned about.

3. Behavior modification: changing attitudes and beliefs towards food and exercise is the most crucial step in

initiating and maintaining weight loss. Family involvement and a sensitive and caring attitude towards the child

is the key to a successful weight loss regimen.

4. Drugs: anorectic agents are not preferred in management of pediatric obesity. Fluoxetine has been tried in

severe adolescent obesity with some success.

5. Surgery: Jaw wiring and gastric stapling have been tried in morbidly obese adoles-cents with serious medical

complications. Without behavior modification, success rate is very low.

 
 

Prevention of obesity

Learning healthy eating habits, active life style, limiting sedentary habits like TV viewing, computer

games, etc., are basic requirements to a successful preventive program. Parents, schools, health care

professionals, governmental bodies, all need to participate in such a program.

In a nutshell, the approach to childhood obesity calls for detailed history taking, thorough physical

exam, careful search for clues to the underlying disorder, minimum lab investigations and finally a structured

program comprising of behavior modifications, diet guidelines, and exercise. Children need to be handled with

compassion, sensitivity and constant reinforcement and reassurance. Involvement of family, friends, physician

and teachers are mandatory for a long term successful outcome.

Children watching TV: A recent study in JAMA (1998; 279: 938-42) shows that boys and girls who watched TV

for > 4 hours a day had more body fat and a higher body mass index than those who watched for less than two

hours. 

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
DEBATE

 
 
 
 
IDLI versus VADA
 
 
 
 
 
 



 CONTACT EMAIL: indianobesity @rediffmail.com
 
 
DR. PRAVEEN RAMACHANDRA