Child and adolescent obesity: Why we need to fight!

Obesity is well-recognized disease, and childhood obesity is a long-term risk factor for adult morbidity and social disabilities [1,2]. Childhood obesity is not only a risk factor for future adult obesity but it is clearly also connected to complications already during the teenage period giving a rise in maturity-onset diabetes in the young (MODY) [3]. Furthermore, orthopaedic problems, a risk of impaired quality of life, and socially and educationally impaired development might concur [1]. Obesity should be defined as excess body fat. The most widely used measurement to define obesity is the body mass index (BMI) (weight in kilos divided by height in square metres, kg/m). It is a predictor of body fat from a population perspective, but has limitations on an individual level and is only a proxy measurement of body fat [4]. BMI shows significant variations during childhood; that is the reason why ageand gender-specific reference standards must be used. In addition, in adolescents, pubertal status should also be evaluated, since puberty leads to an increase in percent body fat. There is also an increase in cardiovascular risk factors for obese children that might explain the increased risk of mortality from all causes and increased morbidity from coronary heart disease [5]. Furthermore, long-term health complications in overweight children after 40 y follow-up include significantly increased rates of cardiovascular diseases and digestive diseases but also increased mortality [6]. Already as a teenager, the morbidity in type 2 diabetes has increased in certain ethnics groups [7]. The increase of type 2 diabetes in adolescents might be explained by the increase in obesity. However, sedentary lifestyle might increase both the risk for obesity and diabetes (Figure 1). Furthermore, the definition of obesity might be important. The increase in diabetes might be explained by an increase of visceral adiposity and not obesity defined solely by an increase in adipose tissue (Figure 2). We lack reference values in most countries for abdominal adiposity in children. We also lack a definition of visceral adiposity in children. It might be beneficial to make a distinction between visceral adiposity that might be present in both children and adults and early-onset non-visceral adiposity (EONVA) that starts in childhood and can be combined with visceral adiposity. Late-onset visceral adiposity (LOVA) is hypothesized to represent only a small proportion of childhood obesity but a dominating proportion later in life. Early-onset visceral adiposity (EOVA) could be connected to the metabolic syndrome described recently [8]. However, we lack a clear definition of the metabolic syndrome in that paper on childhood obesity [8]. Comparative data on visceral adiposity in children are still lacking but, in a comparative survey using BMI, the rate of obesity in teens in the US is three times higher than in Europe (11–15% vs 5%) [9]. This might indicate that visceral adiposity is more common in children in the US, partly explaining the increase of type 2 diabetes in certain groups [7]. From a public health point of view, we do not want Europe to reach the prevalence of obesity seen in the US. That is why we have to take the necessary steps to support children, families, schools and health professionals to avoid this development.