Environmental Epigenetics, 2016 · DOI: 10.1093/eep/dvw022 · Published: September 16, 2016
Exposure to environmental toxicants, like bisphenol-A (BPA), is a contributing factor to the rise in obesity and metabolic diseases globally. BPA exposure during early life, even in embryonic stages, can increase the likelihood of weight gain and metabolic disturbances like obesity and diabetes later in life. BPA and other endocrine disruptors can change how fat tissue develops, affecting the body's ability to create functional fat cells and influencing their differentiation into specific types. Epigenetic mechanisms play a role in these BPA-induced effects related to obesity, observed in both lab experiments and animal models. Developmental exposure to BPA can lead to abnormalities that are passed down to future generations through a process called transgenerational epigenetic inheritance.
Highlights the need to reduce exposure to BPA and similar endocrine disruptors, especially during sensitive developmental windows, to mitigate the risk of metabolic diseases.
Calls for further research into the mechanisms by which BPA affects precursor cells and alters their differentiation capabilities, as well as the long-term effects of low-dose BPA exposure.
Suggests the need for stricter regulations and guidelines regarding the use of BPA in consumer products to protect public health and prevent transgenerational effects.