Bisphenol A substitutes and obesity: a review of the epidemiology and pathophysiology

Abstract

The prevalence of obesity, a condition associated with increased health risks, has risen significantly over the past several decades. Although obesity develops from energy imbalance, its etiology involves a multitude of other factors. One of these factors are endocrine disruptors, or “obesogens”, when in reference to obesity. Bisphenol A (BPA), a known endocrine disruptor used in plastic materials, has recently been described as an environmental obesogen. Although BPA-free products are becoming more common now than in the past, concerns still remain about the obesogenic properties of the compounds that replace it, namely Bisphenol S (BPS), Bisphenol F (BPF), and Bisphenol AF (BPAF). The purpose of this review is to investigate the relationship between BPA substitutes and obesity. Literature on the relationship between BPA substitutes and obesity was identified through PubMed and Google Scholar, utilizing the search terms “BPA substitutes”, “bisphenol analogues”, “BPS”, “BPF”, “BPAF”, “obesity”, “obesogens”, “adipogenesis”, “PPARγ”, and “adipocyte differentiation”. Various population-based studies were assessed to gain a better understanding of the epidemiology, which revealed evidence that BPA substitutes may act as obesogens at the pathophysiological level. Additional studies were assessed to explore the potential mechanisms by which these compounds act as obesogens. For BPS, these mechanisms include Peroxisome proliferator-activated receptor gamma (PPARγ) activation, potentiation of high-fat diet induced weight-gain, and stimulation of adipocyte hypertrophy and adipose depot composition. For BPF and BPAF, the evidence is more inconclusive. Given the current understanding of these compounds, there is sufficient concern about exposures. Thus, further research needs to be conducted on the relationship of BPA substitutes to obesity to inform on the potential public health measures that can be implemented to minimize exposures.

Sex and Gender Differences on the Impact of Metabolism-Disrupting Chemicals on Obesity: A Systematic Review

“…Overall, the combined data suggest that prenatal exposure to PBDE, phenols, phthalates and parabens recognized as MDCs may affect sex-specific body fat distributions in children due to the chemical interaction with steroid glucocorticoid and PPAR receptors, which are involved in AT distribution and function [ 81 , 82 ]. Furthermore, the higher body fat percentage in girls at birth and during adolescence supports their increased vulnerability to MDC effects [ 83 , 84 ].…”

Impact of combined chronic exposure to low-dose bisphenol A and fructose on serum adipocytokines and the energy target metabolome in white adipose tissue

“…6 In addition, several previous studies have investigated this effect, and the activation of PPARγ and its downstream genes may be the mechanistic link. 21 However, studies that provide detailed information on the changes in adipose tissue caused by combined exposure to BPA and fructose are limited.…”