Reacción a "Prenatal exposure to a mixture of endocrine disruptors is associated with poorer metabolic health in childhood"

The prevalence of abdominal obesity, elevated blood pressure, inadequate lipid levels and hyperglycaemia, all components of the metabolic syndrome (MetS), is increasingly prevalent in children. These early clinical manifestations in turn increase the risk of cardiovascular disease in adulthood. In order to implement effective preventive measures, it is necessary to understand the origin and development of obesity and metabolic syndrome and to identify the associated modifiable risk factors. 

Güilt-Oumrait's work, published in JAMA Network Open, explores the origin of metabolic syndrome in childhood, investigating the role of early exposure (preconception, prenatal and early life) to four families of chemicals (metals and organohanohalogen compounds - chlorinated, brominated and perfluorinated) in this disease. The researchers found that high maternal exposure to these obesogenic pollutants was associated with a significantly increased risk of metabolic syndrome in children aged 6-11 years in the Human Early Life Exposome (HELIX) population cohort.  

Toxicological data indicate that the selected chemical families can induce adverse multisystemic metabolic effects. For example, perfluorinated compounds (PFAS) accumulate in the liver, contributing to fatty liver and dyslipidaemia, and some organochlorine compounds, accumulated in adipose tissue, are associated with obesogenic and diabetogenic effects. 

The authors also included in this work clinical metabolic markers measured in the children's serum and urine, which reinforced and explained the results found. Moreover, since the diagnosis of MS in children is not an easy task, the authors propose a ‘risk score’ to facilitate the identification of clinical MS in childhood before it appears. The variables finally included in the proposed score were waist circumference, systolic and diastolic blood pressure, triglyceride, HDL-cholesterol and insulin levels, which allowed them to identify the most at-risk population of children.  

The work of Güilt-Oumrait et al. therefore: 

1. It represents a solid advance in the epidemiological and toxicological knowledge of the health consequences of early (in utero) exposure to mixtures of chemical-persistent substances that can alter the metabolic programming of the infant population. 
2. It allows the identification of particularly vulnerable populations. 
3. It allows the establishment of preventive measures in children at high cardiovascular risk.  

Although observational studies do not allow to establish definitive causes, the consistency of in vitro, in vivo and epidemiological data strongly argues for the need to reduce exposure to chemical-obesogenic compounds and/or metabolic disruptors, especially in women of childbearing age and during the first years of life (children).