Role of nutrition and environmental endocrine disrupting chemicals during the perinatal period on the aetiology of obesity.
The basis for the current obesity epidemic remains controversial. However, the simplistic idea that obesity can be explained by two factors: energy intake and energy expenditure, is now being challenged due to the lack of success in decreasing obesity based on a focus on only these two factors. In this article we propose an emerging hypothesis that the recent dramatic increase in obesity could be due to developmental nutrition, developmental exposure to environmental chemicals or the interaction of nutrition and environmental chemical exposures during development. Indeed, developmental exposure to environmental chemicals in animal studies has been shown to increase the susceptibility to a number of diseases including obesity. Obesity is thus one of many diseases shown to have a developmental origin. We show that factors that impact growth during fetal and neonatal life, such as placental blood flow and nutrient transport to fetuses, as well as components of the maternal and infant diets, can influence weight gain later in life. In addition, we show that developmental exposure to endocrine disrupting chemicals can create abnormalities in homeostatic control systems required to maintain a normal body weight throughout life. Eliminating exposures to these chemicals and improving nutrition during development offer the potential for reducing obesity and associated diseases.
Division of Extramural Research and Training, National Institute of Environmental Health Sciences, NIH/DHHS, Cellular, Organs and Systems Pathobiology Branch, Research Triangle Park, NC 27709, USA. heindelj@niehs.nih.gov
Jerrold J
JJ
Heindel
Frederick S
FS
vom Saal
D000818:Animals; D004032:Diet; D052244:Endocrine Disruptors / Q000494:pharmacology*; D004781:Environmental Exposure; D004785:Environmental Pollutants / Q000494:pharmacology*; D005260:Female; D005333:Fetus / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D009538:Nicotine / Q000009:adverse effects; D009752:Nutritional Status; D009765:Obesity / Q000209:etiology*; D010920:Placenta / Q000098:blood supply / Q000502:physiology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012039:Regional Blood Flow
D052244:Endocrine Disruptors; D004785:Environmental Pollutants; D009538:Nicotine