written by Sarah Howard
CHE Diabetes-Obesity Spectrum Working Group Coordinator
A review article on prenatal exposure to endocrine disrupters and obesity was just published. Overall, it found that, “For certain EDCs, early life exposure may be associated with weight homeostasis later in life, however not necessarily in an obesogenic direction.” The review includes both human and laboratory evidence (19 studies) published since 1995. (The review did not include studies on BPA.) Here are their findings for the chemical classes included:
Organotins are well-documented obesogens in laboratory studies. Human studies, however, are not available. Prenatal exposure to tributyltin causes adioposity in exposed mice, and these effects may be transmitted to future generations as well.
Persistent organic pollutants (POPs)
Human studies of prenatal exposure to POPs show conflicting results. Several studies show no association between PCB exposure and growth measurements, and while other studies do, associations are both positive and negative. However, several studies do show positive associations between prenatal DDE exposure and later BMI. The authors conclude that “Evidence in support of a significant association between prenatal exposure to PCBs or DDE and decreased or increased weight gain later in life, seems unconvincing.”
Brominated flame retardants
In experimental studies, high levels of BFRs can affect growth and metabolism. Some human studies have found negative associations between BFR exposure and birth weight, but there are no studies yet on growth later in life.
Animal studies of prenatal exposure to environmentally-relevant and higher levels of phthalates show obesogenic effects. Longitudinal human studies are lacking, however.
Perfluorinated alkyl acids
Animal studies of PFOS and PFOA are limited, while human studies are conflicting.
None of the studies in this review found a negative association between prenatal EDC exposure and later-life BMI, and several showed positive associations. Consistent with endocrine disruption, a number of studies showed non-linear dose-response curves, as well as sex-specific differences.
The authors conclude that, “literature does suggest that early life exposure to certain EDCs is associated with weight homeostasis and growth later in life, however not necessarily in an obesogenic direction.” They note that there is a lack of consistence as well as a lack of human data. They suggest that future research should stratify results by gender, include not only BMI but other more sensitive measures of adiposity, such as fat mass, measure exposures prenatally, and follow-up in the long term.
de Cock M, van de Bor M. Obesogenic effects of endocrine disruptors, what do we know from animal and human studies? Environ Int. 2014 Sep;70:15-24. doi: 10.1016/j.envint.2014.04.022. Epub 2014 May 28.
BACKGROUND: Hormonal actions and activation of receptors involved in adipogenesis and brain development during the prenatal period may be affected by exposure to certain chemicals. Experimental studies have shown that amongst others polychlorinated biphenyl (PCB)-153 and dichlorodiphenyltrichloroethane (DDT) may have obesogenic effects in prenatally exposed mice.
OBJECTIVE: To provide an overview of five classes of chemicals which have frequently been indicated as potential obesogens, and to discuss the evidence available regarding early life exposure to these compounds and overweight later in life.
METHODS: Pubmed was systematically searched for publications which related early life exposure to endocrine disrupting chemicals (EDCs) to growth parameters later in life. We included 19 studies, which were published from 1995 and onwards.
RESULTS: Both positive and negative associations are observed between early life exposure and weight or height at various ages, including as early as 14 months, as well as until 20 years of age. In none of the included studies negative associations between perinatal exposure to EDCs and body mass index (BMI) were found and in several studies a positive association was observed. Dose-response relations appear to be non-monotonic.
CONCLUSION: For certain EDCs, early life exposure may be associated with weight homeostasis later in life, however not necessarily in an obesogenic direction. More sensitive measures of adiposity as well as long-term follow-up are warranted for future studies.