Organic Consumers Association

Campaigning for health, justice, sustainability, peace, and democracy

No Guarantees: Studies Shed New Light on the EDC Potential of BPA & BPS

While bisphenol A is a known endocrine-disrupting compound (EDC), its substitute bisphenol S has been shown to be worrisome as well. Three new studies add more evidence that exposure to these EDCs early in life will likely lead to serious health issues later in life.

Once again, bisphenol A (BPA) is making headlines, and, as always, not in a good way. Hundreds of epidemiological studies have been published that link BPA, a known endocrine-disrupting compound (EDC) even at very low doses, to health problems affecting all human body systems. Two new studies raise yet more cause for alarm, and a third demonstrates that a commonly used BPA substitute is probably not much better for human health. Collectively, these studies contribute to the burgeoning body of evidence that exposure to EDCs during critical developmental periods predisposes the individual to serious disease.

Once again, bisphenol A (BPA) is making headlines, and, as always, not in a good way. Hundreds of epidemiological studies have been published that link BPA, a known endocrine-disrupting compound (EDC) even at very low doses, to health problems affecting all human body systems. Two new studies raise yet more cause for alarm, and a third demonstrates that a commonly used BPA substitute is probably not much better for human health. Collectively, these studies contribute to the burgeoning body of evidence that exposure to EDCs during critical developmental periods predisposes the individual to serious disease.

BPA and Obesity

In “Perinatal Exposure to Low-Dose Bisphenol-A Disrupts the Structural and Functional Development of the Hypothalamic Feeding Circuitry,” published in Endocrinology, Alfonso Abizaid, PhD, of Carleton University in Ottawa, Canada, and team followed up on existing studies that demonstrated how exposure to BPA in the early postnatal period affects body weight, glucose homeostasis, and liver function in mice to confirm that the metabolic impairments were the result of the exposure rather than a function of their postnatal environment or a certain metabolic phenotype.

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