1,721,407 research outputs found
Aetiology of overweight and obesity in children and adolescents.
No full textThe epidemic diffusion of obesity in industrialised countries has promoted research on the aetiopathogenesis of this disorder. The purpose of this review is to focus mainly on the contribution that European research has made to this field. Available evidence suggests that obesity results from multiple interactions between genes and environment. Parents obesity is the most important risk factor for childhood obesity. Twin, adoption, and family studies indicated that inheritance is able to account for 25% to 40% of inter-individual difference in adiposity. Single gene defects leading to obesity have been discovered in animals and, in some cases, confirmed in humans as congenital leptin deficiency or congenital leptin receptor deficiency. However, in most cases, genes involved in weight gain do not directly cause obesity but they increase the susceptibility to fat gain in subjects exposed to a specific environment. Both genetic and environmental factors promote a positive energy balance which cause obesity. The relative inefficiency of self-adapting energy intake to energy requirements is responsible for fat gain in predisposed individuals. The role of the environment in the development of obesity is suggested by the rapid increase of the prevalence of obesity accompanying the rapid changes in the lifestyle of the population in the second half of this century. Early experiences with food, feeding practices and family food choices affect children's nutritional habits. In particular, the parents are responsible for food availability and accessibility in the home and they affect food preferences of their children. Diet composition, in particular fat intake, influences the development of obesity. The high energy density and palatability of fatty foods as well as their less satiating properties promotes food consumption. TV viewing, an inactivity and food intake promoter, was identified as a relevant risk factor for obesity in children. Sedentarity, i.e. a low physical activity level, is accompanied by a low fat oxidation rate in muscle and a low fat oxidation rate is a risk factor of fat gain or fat re-gain after weight loss. Conclusion: Further research is needed to identify new risk factors of childhood obesity, both in the genetic and environmental areas, which may help to develop more effective strategies for the prevention and treatment of obesity
Level of physical activity and adiposity in children: relevance of sedentary behaviors.
No full textThis is a letter to authors (Ekelund U et al. Am J Clin Nutr 2004;80:584-90), in which is commented the weakness of the conclusion of the article, which apparently reduces the relevance of the intensity of physical activity in the maintenance of childhood obesity and seems to frustrate the reasonable expectancy for the role potentially played by exercise and physical activity both in the prevention and treatment of overweight. Moreover, it is underlined that, at present, a change from sedentary behavior to a more active lifestyle remains a cornerstone of strategies to prevent and treat childhood obesity
Physical activity in the prevention and treatment of childhood obesity: physio-pathologic evidence and promising experiences.
No full textPhysical activity is a cornerstone of both prevention and treatment of childhood obesity. Skeletal muscle is a powerful fat oxidizer and its role in daily fat balance is crucial. Training increases fat oxidation rate both during exercise and in resting conditions. Reduction of physical activity promotes fat gain and vice versa. Data on obese adults showed a reduced mitochondrial oxidative capacity, which is partially reversible, by increasing physical activity. Available data demonstrate that reducing sedentary behaviour (video-exposition) and promoting light activity (walking) is helpful in promoting weight control in children. Moreover, especially in older children and adolescents, an increase of moderate-to-vigorous physical activity seems to be promising. Nevertheless, further studies are still necessary to design more effective preventive and treatment programs for childhood obesity
Childhood obesity: the genetic-environmental interface.
No full textObesity has a high prevalence in children living in industrialized countries. Excess adiposity is the result of a prolonged positive energy balance. Both genetic and environmental factors are involved. A genetic predisposition to obesity has been ascertained from, for example, twin studies. Animal models of genetic obesity have been used to identify candidate genes, which have, in some cases, also been demonstrated in humans. Genome scanning has highlighted some of the human genes that may be involved. Several environmental factors promote an imbalance between nutrient intake and nutrient oxidation in genetically predisposed children. Fat intake is associated with adiposity in children. The low thermogenesis induced by fat intake is another potential contributory factor. Oxidative activity in skeletal muscles greatly influences total energy expenditure as well as fat oxidation rate. Sedentary behaviour promotes low energy requirements in children. Moreover, low skeletal muscle activity reduces fat oxidation, favouring fat gain. Several socio-economic and cultural factors affect the dietary and physical activity habits of children. Finally, the enlargement of the fat mass induces compensatory metabolic reactions to oppose further fat gain. Further research on the factors responsible for the pathogenesis of obesity is necessary to identify more sensitive targets for the effective prevention and treatment of childhood obesity
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