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OBesogenic Endocrine disrupting chemicals: LInking prenatal eXposure to the development of obesity later in life

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Weighing up the origins of obesity

A European study examined if the origins of childhood obesity are present before birth. In this context, they evaluated the effect of a number of endocrine disrupting compounds (EDCs).

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The incidence of childhood obesity has reached epidemic proportions globally. Despite advancements in knowledge on the endocrine and neuronal regulation of energy balance, the underlying mechanisms of obesity remain unclear. Accumulating evidence suggests that determinant factors act early in life and exposure to environmental contaminants increases the susceptibility to obesity. The EU-funded OBELIX (Obesogenic endocrine disrupting chemicals: linking prenatal exposure to the development of obesity later in life) project examined the hypothesis that prenatal exposure to EDCs in food plays a role in the development of obesity later in life. The project focused on six major classes of EDCs, namely dioxins, polychlorinated biphenyls, brominated flame-retardants, organochlorine pesticides, phthalates, and perfluorinated alkyl acids (PFAAs). Using birth cohorts across Europe, scientists observed that perinatal EDC exposure is widespread. They developed novel methods for assessing the presence of chemicals in cord blood and breast milk. Following epidemiological assessment of birth weight, growth, body mass index (BMI) in children, they found that postnatal exposure to PCB 153 was related to reduced birth weight. Prenatal dichlorodiphenyldichloroethylene (DDE) was associated with rapid growth in children up to 2 years of age while perinatal exposure to dioxin-like chemicals elevated BMI. In another part of the project, scientists performed animal studies to support their epidemiological observations. Perinatal exposure of mice to various EDCs resulted in altered lipid levels and metabolic disturbance, which however did not consistently coincide with an increase in body weight. Insight into the EDC mechanism of action indicated epigenetic and gene expression changes concomitant with fat cell differentiation. Additional studies in cord blood showed an association with glucocorticoid, oestrogen and progesterone signalling. Furthermore, risk assessment revealed that critical effect concentrations of certain EDCs were lower than those used to set current tolerable daily intake (TDI) levels. As a result, current TDIs might not be sufficiently protective. Taken together, the results of the OBELIX project indicate that early life exposure to EDCs can alter metabolic pathways responsible for weight regulation. However, the long-term consequences of these effects in early childhood warrant further investigation.


Obesity, endocrine disrupting compounds, prenatal exposure, lipid, gene expression

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