Obesity in the adolescent.

Abstract

The industrialized countries around the world are experiencing an epidemic of obesity. The level of fatness of an adolescent at which morbidity acutely and/or later in life increases is determined on an individual basis. However overall obesity substantially increases the risk of subsequent morbidity. The genetic basis of obesity has been elucidated to some extent through the discovery of leptin the ob gene product and the increasing knowledge on the role of neuropeptides such as proopiomelanocorticotropin POMC neuropeptide Y (NPY) and the melanocyte concentrating hormone receptors. Environmental/exogenous factors largely contribute to the development of a high degree of body fatness early in life. Twin studies suggest that approximately 50% of the tendency toward obesity is inherited. There are numerous disorders including a number of endocrine disorders (Cushings syndrome hypothyroidism etc.) and genetic syndromes (Prader-Labhard-Willi syndrome Bardet Biedl syndrome etc.) that can present with obesity. A simple diagnostic algorithm allows for the differentiation between primary or secondary obesity. Among the most common sequelae of obesity in the adolescent are hypertension dyslipidemia back pain and psychosocial problems. The definition of obesity in childhood and adolescence is not easy. However body mass index (BMI) is now generally accepted to be used to define obesity in children and adolescents clinically. An increased risk of death from cardiovascular disease in adults has been found in subjects whose BMI had been greater than the 75th percentile as adolescents. Therapeutic strategies include psychological and family therapy lifestyle/behavior modification and nutrition education. The role of regular exercise and exercise programs is emphasized. (authors)