This was partly due to the fact that even though the children believed they were eating less their actual calorie consumption did not decrease with the intervention. At the same time observed energy expenditure remained similar between the groups. This occurred even though dietary fat intake decreased from 34% to 27%. A second study of 5,106 children showed similar results. Even though the children ate an improved diet there was no effect found on BMI. Why these studies did not bring about the desired effect of curbing childhood obesity has been attributed to the interventions not being sufficient enough. Changes were made primarily in the school environment while it is felt that they must occur in the home, the community, and the school simultaneously to have a significant effect.A Cochrane review of a lower fat diet in children (30% or less of total energy) to prevent obesity found the existing evidence of very low to moderate quality, and firm conclusions could not be made.Calorie-rich drinks and foods are readily available to children. Consumption of sugar-laden soft drinks may contribute to childhood obesity. In a study of 548 children over a 19-month period the likelihood of obesity increased 1.6 times for every additional soft drink consumed per day.Calorie-dense, prepared snacks are available in many locations frequented by children. As childhood obesity has become more prevalent, snack vending machines in school settings have been reduced by law in a small number of localities.
Genetics
Childhood obesity is often the result of an interplay between many genetic and environmental factors. Polymorphisms in various genes controlling appetite and metabolism predispose individuals to obesity when sufficient calories are present. Over 200 genes affect weight by determining activity level, food preferences, body type, and metabolism. Having two copies of the allele called FTO increases the likelihood of both obesity and diabetes.As such, obesity is a major feature of a number of rare genetic conditions that often present in childhood:

Prader–Willi syndrome with an incidence between 1 in 12,000 and 1 in 15,000 live births is characterized by hyperphagia and food preoccupations which leads to rapid weight gain in those affected. Bardet–Biedl syndrome
MOMO syndrome
Leptin receptor mutations
Congenital leptin deficiency
Melanocortin receptor mutationsIn children with early-onset severe obesity (defined by an onset before ten years of age and body mass index over three standard deviations above normal), 7% harbor a single locus mutation.One study found that 80% of the offspring of two obese parents were obese in contrast to less than 10% of the offspring of two parents who were of normal weight. The percentage of obesity that can be attributed to genetics varies from 6% to 85% depending on the population examined. Family practices
In the recent decades, family practices have significantly changed, and several of these practices greatly contribute to childhood obesity:
With a decreasing number of mothers who breast-feed, more infants become obese children as they grow up and are reared on infant formula instead.