Until recently, paediatricians in most parts of the world took little interest in the problem of childhood obesity because it was an unusual condition, often associated with such genetic disorders as the Prader-Willi syndrome or occurring in response to severe brain damage during childbirth. Occasional children coming from exceptionally disturbed families were also affected, but there was not much clinical interest because the handicap of being obese were either psychological from being seen to be abnormal or the skeletal consequences of gross overweight in a growing child. Any European country had therefore only one or two paediatricians providing national expertise; a host of other more urgent medical problems dominated paediatric priorities. Only in the United States (US) was there greater interest, perhaps conditioned not only by the greater frequency of childhood obesity in the 1970s and early 1980s, but also because of the dominant role of paediatricians in the routine care of children.
The prevalence of childhood obesity has increased during the past decades in industrialized countries . This is not surprising because children and adolescents have become heavier at a rate of about 0.2 kg per year in recent times. This trend is worrisome because obese children often grow into obese adults . Harmful metabolic consequences of obesity may be evident in childhood and even a young obese child may suffer from serious morbidities . A study conducted in Muscatine, Iowa, USA, revealed that clustering of obesity in families is related to the clustering of coronary risk factors in children and their relatives . The identification of children at risk of becoming obese adults offered the opportunity to prevent or delay the onset of the disease through appropriate intervention. Thus, it is important to identify the factors that contribute to obesity in childhood. The observation that children of obese parents are more likely to become obese early in life suggests that inherited factors are involved in the predisposition to childhood obesity. This notion is reinforced by the fact that a low but significant relationship exists between parental and offspring fatness even when children are reared apart from their biological parents . Thus, the familial aggregation of adiposity cannot be only attributed to a common lifestyle and exposure to the same environment. Indeed, data also support the hypothesis that shared genetic characteristics also contribute to obesity risk.
The World Health Organization has called obesity a global epidemic . Indeed, its prevalence is increasing worldwide at alarming rates in adults and children . This marked and rapid increase in the prevalence of obesity is found in affluent countries, in countries in economic transition and in developing countries. This increase in prevalence in all settings suggests the important contributions of both exogenous factors in addition to genetic predisposition . The identification of contributing factors is important because obesity in children has marked adverse effects in childhood, adolescence and adulthood. Its ad-verse long-terra effects extend well into adulthood. Obese children tend to suffer from psychosocial distress and, in many environments, from considerable discrimination. Long-term prospective studies of obese adolescent females indicate that they achieve fewer years of education, and in adulthood have higher rates of poverty, lower rates of marriage and less household income than do those who were normal weight in adolescence [4, 5]. Obesity negatively influences cardiovascular risk factors such as dyslipidaemia, glucose intolerance and arterial hypertension. Dyslipidemia characterized by increased concentrations of plasma triglycerides and low density lipoprotein (LDL) cholesterol, and reduced high density lipoprotein (HDL) cholesterol concentrations, is a common finding in young obese children [6, 7]. Obesity induces reduced insulin sensitivity, pathological glucose tolerance and increased fasting as well as post-prandial blood glucose concentrations.
The epidemiology of obesity strongly suggests that environmental determinants, particularly those found within families, are significant in both the aaetiology and treatment of childhood obesity. Family and other social environmental influences interact with genetic predispositions to childhood obesity. Several studies showed that risk factors for weight gain in school age children are linked strongly to low physical activity and family environmental factors [1-3]. The family is the primary source of environmental factors that determine energy balance in young children. Indeed, a child with a genetic predisposition to obesity who lives in a social environnent in which energy-dense foods are easily accessible and whose family tends to be sedentary is at increased risk for obesity [3, 4] than a similarly genetically predisposed child who lives with a physically active family with a more healthful diet.
Obesity is one of the most common health problems in affluent societies. It is associated with increased risk of morbidity and mortality such as non-insulin dependent diabetes (NIDDM or type II diabetes), hypertension and cardiovascular disorders, and other physical and psychosocial consequences . This is particularly important in the light of dramatic increases in in the past thirty years in adiposity and excess body weight relative to height in young children and adolescents . More-over, as incomes rise and populations become more urban in emerging economies, diseases of nutrition excess become increasingly more common relative to nutrition deficiencies- a phenomenon called the "nutrition transition".