Childhood obesity

• Twin and adoption studies show clear evidence of a role for genetic factors which is variously estimated to be between 25% and 40%, but the precise genes involved have not been identified. The predisposition for obesity clearly exists in a minority of the population.
• A variety of single gene defects have been identified for animals and some of them have been shown to exist in humans as well. However, single gene defects are rare, if not exceptional cases and the overwhelming cause in the majority of obese children can be traced to lifestyle factors
• Leptin is the product of the ob gene and it has been shown to be involved in a few, very rare cases of extreme childhood obesity. The ob gene defects demonstrate a susceptibility or probability of excessive intake, but it is likely that other genes determine energy expenditure through effects on metabolic efficiency or physical activity.
• All these genetic deficiencies are associated with excessive appetite and overeating, leading to the development of gross obesity from an early age. Genes must act by modulating either intake or expenditure of energy and thus can only convey an increased likelihood of becoming obese, or conversely remaining lean. In addition, genetic factors cannot explain the recent rise in the prevalence of obesity. Genetics can load the gun but lifestyle factors must pull the trigger!

• Studies  into the impact of parental eating and exercise habits on the risk of obesity in children, show similarity between parents and children in both these habits.  The  associations are strongest for younger children, becoming weaker through adolescence as outside influences take over and the child becomes more independent.
• Young children of active parents were two to three times as likely to be active as children of inactive parents and if both parents were active there was a 7-fold increase.  Do parents act just act as role models for their children, or do they share in their activities and facilitate their children's activity? Probably both.

• Cross-sectional studies in children have mostly failed to find a significant correlation between total energy intake and fatness, but these studies are confounded by evidence of under-reporting of food intake.
• Studies which have examined the contribution of individual nutrients e.g. fat and sugar, or the frequency of eating (snacking) have also been inconclusive. This may reflect the lack of a true association or methodological difficulties in conducting these studies. Inaccurate and unreliable energy intake measurements may well have generated misleading hypotheses about the origins of childhood obesity.

• There is evidence from diverse sources of a decline in the level of habitual physical activity in the population at large, including children, and an increase in sedentary lifestyles. For example, less than 5% of children cycle to school.  Walking to school has decline from around 50% to 35% in favour of transport by car.  Additionally, the time devoted to physical education in schools has declined and the time spent watching TV and video's has increased.

• Endocrine problems (Usually have short stature or faltering growth):
• Hypothyroidism (particularly in Down’s syndrome)
• Cushing’s syndrome (truncal obesity, hypertension, hirsutism, purple striae)
• Growth hormone deficiency (may have weight gain and delayed puberty)
• Chromosomal abnormalities e.g. Prader-Willi (poor linear growth, developmental delay, small genitalia, dysmorphic).
• Drug related e.g. steroids

• Spina bifida
• Muscular dystrophy
• Other causes of immobility
• Polycystic ovarian syndrome