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 cachexi