title: Programming towards childhood obesity.
abstract: There is now considerable evidence that a constitutional susceptibility to fat gain is necessary for children to become obese under the pressure of an obesogenic environment; this is the programming towards obesity. The role of genetics in this programming is dominant. Besides the rare monogenic recessive forms of obesity secondary to mutations in genes involved in the hypothalamic appetite control pathways, obesity linked to mutations in melanocortin 3 and 4 receptors are more frequent due to their dominant mode of transmission. Predisposition to common obesity is polygenic and involves a network of genes; nevertheless, more research is required to elucidate their exact role. Fetal and perhaps early postnatal programming is also possible. Under- and overnutrition, diabetes, and maternal smoking during pregnancy were shown to promote later obesity and may affect the central body weight regulatory system during fetal development. The role of early postnatal factors such as formula-feeding rather than breastfeeding, excess in n-6 polyunsaturated fatty acids or protein intakes, and excessive weight gain early in life is more questionable and needs further investigation. Taking into consideration that childhood obesity is a programmed disease should modify its clinical management. Childhood obesity should no longer be considered as the result of inappropriate eating habits and/or excessive inactivity in order to relieve the obese children's discrimination and their parents' guilt. Since treatment of obese children requires a substantial motivation to continuously fight against the programmed excessive drive to eat, it seems wiser to wait for children to be old enough, thus more motivated, to initiate energy restriction. Moreover, with the great majority of children being not predisposed to obesity, prevention strategies should not be addressed to the whole pediatric population but targeted to those children at risk. Improvement of knowledge on programming towards obesity is essential to develop more promising therapeutic and preventive approaches.
authors.affiliation: Department of Pediatric Nutrition, Armand Trousseau Hospital, Paris, France. p.tounian@trs.aphp.fr
authors.forename: Patrick
authors.initials: P
authors.lastname: Tounian
mesh_terms: D000293:Adolescent; D015992:Body Mass Index; D002648:Child; D002675:Child, Preschool; D044127:Epigenesis, Genetic; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D007223:Infant; D041943:Infant Formula; D007231:Infant, Newborn; D008019:Life Style; D039382:Maternal Nutritional Physiological Phenomena; D009765:Obesity / Q000209:etiology* / Q000235:genetics* / Q000517:prevention & control; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D044105:Receptor, Melanocortin, Type 4 / Q000235:genetics; D012307:Risk Factors; D015430:Weight Gain / Q000235:genetics / Q000502:physiology
chemical_list: C470072:MC4R protein, human; D044105:Receptor, Melanocortin, Type 4